ライフサイエンスコーパス: visceral

1 1), and disease involvement (visceral vs non-visceral).

2 ity fat fraction [PDFF] and subcutaneous and visceral abdominal fat).

3 ave 12% to 14% longer risk-adjusted pLOS for visceral abdominal surgery, independent of patient compl

4 pocytes induces free fatty acid release from visceral adipocytes, thereby promoting obesity-induced h

5 -like thermogenic adipocytes within multiple visceral adipose depots.

6 Zfp423 deletion in fetal visceral adipose precursors (Zfp423(l)(oxP/loxP); Wt1-Cr

7 d to enhanced insulin signaling in liver and visceral adipose tissue (epididymal white adipose tissue

8 muscle (r = 0.825; P = .003), and abdominal visceral adipose tissue (r = 0.820; P = .004).

9 maging and spectroscopy were used to measure visceral adipose tissue (VAT) and liver fat fraction (LF

10 The effect of visceral adipose tissue (VAT) and subcutaneous adipose t

11 ciation of habitual SSB intake and change in visceral adipose tissue (VAT) and subcutaneous adipose t

12 Subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) are associated with advers

13 tion of non-canonical WNT5A/PCP signaling to visceral adipose tissue (VAT) inflammation and associate

14 ntervention on food intake, body weight, and visceral adipose tissue (VAT) mass; plasma, lipids (chol

15 d expression of some adipogenesis markers in visceral adipose tissue (VAT) of HFD-fed M-JAK2(-/-) mic

16 Chronic inflammation in visceral adipose tissue (VAT) precipitates the developme

17 In visceral adipose tissue (VAT), HFD exposure determined a

18 formation, we used a novel ex vivo system of visceral adipose tissue (VAT)-condition medium-stimulate

19 ibution, and the main specific end point was visceral adipose tissue (VAT).

20 mote the resolution of inflammation in human visceral adipose tissue from obese (Ob) patients.

21 ific CD1d deletion decreased the size of the visceral adipose tissue mass and enhanced insulin sensit

22 vanced ovarian cancer usually spreads to the visceral adipose tissue of the omentum.

23 bers were decreased in both subcutaneous and visceral adipose tissue of TRPC1 KO mice fed a HF diet a

24 est that TNMD acts as a protective factor in visceral adipose tissue to alleviate insulin resistance

25 significant differences in subcutaneous and visceral adipose tissue volumes and ratios.

26 eding reduces senescent phenotype markers in visceral adipose tissue while attenuating physical impai

27 The omentum is a visceral adipose tissue with unique immune functions.

28 ndependent of coronary artery calcium score, visceral adipose tissue, and 10-year global cardiovascul

29 tion of limb and trunk fat, subcutaneous and visceral adipose tissue, and increased total cholesterol

30 propria (LP) of the small intestine, brain, visceral adipose tissue, bone marrow (BM), spleen, and t

31 y molecules from other tissues, particularly visceral adipose tissue, can also induce muscle inflamma

32 minal subcutaneous adipose tissue, increased visceral adipose tissue, marked IR, dyslipidemia, and fa

33 of tdTomato-C3aR in the brain, lung, LP, and visceral adipose tissue, whereas it was minor in the spl

34 Visceral adipose tissue-derived serpin (vaspin), serpin

35 nd constitutively at mucosal surfaces and in visceral adipose tissue.

36 d secretory phenotype (SASP) specifically in visceral adipose tissue.

37 er 90-day mortality than patients with lower visceral adipose tissue/subcutaneous adipose tissue (log

38 eous adipose tissue than in those with lower visceral adipose tissue/subcutaneous adipose tissue (p =

39 Sepsis patients with higher visceral adipose tissue/subcutaneous adipose tissue had

40 apy, and ICU stay in patients in the highest visceral adipose tissue/subcutaneous adipose tissue quar

41 t covariates using Cox regression, increased visceral adipose tissue/subcutaneous adipose tissue quar

42 os of 2.01 (95% CI, 1.01-3.99) for the third visceral adipose tissue/subcutaneous adipose tissue quar

43 and 2.32 (95% CI, 1.15-4.69) for the highest visceral adipose tissue/subcutaneous adipose tissue quar

44 e levels was greater in patients with higher visceral adipose tissue/subcutaneous adipose tissue than

45 5, after adjustment for changes in weight or visceral adipose tissue].

46 Incubation of inflamed Ob visceral adipose tissues and human macrophages with RvD1

47 ased Wnt expression in both subcutaneous and visceral adipose tissues and impaired adipogenic differe

48 nt for more than 20% of stromal cells within visceral adipose tissues; however, their functions in th

49 y to lymph nodes (LNs) (i.e., perinodal) and visceral adipose.

50 This finding suggests a link between visceral adiposity and immune aging.

51 the established effects of GCs in increasing visceral adiposity and in reducing thermogenesis, we ass

52 differentially affect the ability to reverse visceral adiposity and metabolic syndrome.

53 Visceral adiposity confers significant risk for developi

54 The visceral adiposity index (VAI), lipid accumulation produ

55 The accumulation of visceral adiposity is strongly associated with systemic

56 s in the elderly is accompanied by increased visceral adiposity, lower exercise capacity, failure to

57 rtly explained by the metabolic syndrome and visceral adiposity, suggesting a possible specific contr

58 se is associated with bone loss and enhanced visceral adiposity.

59 temic inflammation typically associated with visceral adiposity.

60 , partly due to volume overload and variable visceral adiposity.

61 lood pressure control and the development of visceral adiposity.

62 immunohistochemistry for markers of various visceral afferent and efferent systems with c-Fos-based

63 Such segregation means that visceral afferent information followed separate lines to

64 amygdala, is considered to rely on embedded visceral afferent information, although few details are

65 mmation, in the dermatome that overlaps with visceral afferent innervations.

66 activation profiles mean that these parallel visceral afferent pathways encode viscerosensory signals

67 we examined the synaptic characteristics of visceral afferent pathways to the central nucleus of the

68 ironment, that has the capacity to stimulate visceral afferents and facilitate neuronal TRPV1 signali

69 tract, the target of nodose ganglion-derived visceral afferents.

70 Fish skin gelatin was hydrolysed by visceral alkaline-proteases from Giant catfish, commerci

71 direct drug discovery efforts towards novel visceral analgesics.

72 Identification of factors that mediate visceral and bone metastatic spread and subsequent bone

73 Midline thalamus is implicated in linking visceral and exteroceptive sensory information with beha

74 information from the periphery and regulates visceral and immune activity to maintain internal homeos

75 usually presents as early-onset progressive visceral and neurologic disease.

76 , delaying neurodegeneration, and decreasing visceral and neurological cholesterol burden.

77 as evidenced by diseases exhibiting comorbid visceral and psychiatric symptoms.

78 We have highlighted differences in visceral and subcutaneous WAT thermogenic metabolism and

79 e adipose tissue, although glucose uptake in visceral and subcutaneous white adipose tissue depots wa

80 29) but not after additional adjustments for visceral and total body fat.

81 areas contributing to generating and mapping visceral arousal states.

82 gion, contributing to mapping and generating visceral arousal states.

83 frequently intestinal necrosis and multiple visceral arterial aneurysms.

84 ion, and stent implantation into aorto-iliac/visceral arteries and the vena cava (temporal resolution

85 first case reported of infected aneurysms of visceral arteries caused by Group B streptococcus infect

86 ry aneurysms (HAAs) constitute 14% to 20% of visceral artery aneurysms.

87 Phantom visceral artery cannulation was easier with standard and

88 transcriptome analysis comparing mesenteric visceral AT (vAT) of HF and HF/DDE groups revealed a dec

89 osing bilateral sclerites and a deep ventral visceral cavity, these features indicate an affinity wit

90 provides viscerosensory signals to CeA about visceral conditions with respect to being either 'normal

91 r identities, we paired information based on visceral connectivity with a cell-type specific marker o

92 entromedial module deals preferentially with visceral control, affect, and short-term memory, whereas

93 at is just dorsal and caudal to this region (visceral cortex).

94 To elucidate the central encoding of this visceral demand, multisite recordings were made within a

95 ld great promise as potential treatments for visceral disease in NPC patients.

96 sk lesions for tumour flare (eg, >5 sites of visceral disease or bone lesions with impending fracture

97 tivated vs non-activated vs and unknown) and visceral disease status (present vs absent).

98 Randomisation was stratified by visceral disease status.

99 arasites apparently cause both cutaneous and visceral disease, and may have evolved a novel transmiss

100 Using the hamster model of visceral disease, we demonstrate that prior exposure to

101 for advanced breast cancer, and presence of visceral disease.

102 logical conditions, such as tissue damage or visceral distension, induces channel opening, membrane d

103 ments that direct expression in the anterior visceral endoderm (AVE), primitive streak (PS) and defin

104 y a high-fat diet (HFD) has major effects on visceral epididymal adipose tissue (eWAT).

105 ildren with these findings, including 1 with visceral extension to the spleen.

106 re (-4.9 mm Hg; 95% CI, -9.5 to -0.3 mm Hg), visceral fat (-250.19 g; 95% CI, -459.9 to -40.5 g), and

107 oric fructose restriction on DNL, liver fat, visceral fat (VAT), subcutaneous fat, and insulin kineti

108 idence for strong genetic effects underlying visceral fat and android/gynoid ratio.

109 lic effects such as reducing weight gain and visceral fat and increasing glucose-stimulated insulin r

110 at for 3 mo did not differentially influence visceral fat and metabolic syndrome in a low-processed,

111 lipid accumulation in subcutaneous layer and visceral fat and not in the liver.

112 ons, with the strongest associations between visceral fat and Oscillospira members.

113 Measures of visceral fat are positively related to arterial inflamma

114 act electrode system for measuring abdominal visceral fat area (VFA).

115 take, protein intake, physical activity, and visceral fat area, we found that Chinese elderly with T2

116 Individuals with higher measures of visceral fat as well as elevated arterial inflammation a

117 Most of these results involve visceral fat associations, with the strongest associatio

118 2D show a greater propensity for ectopic and visceral fat deposition.

119 and the pathophysiological contributions of visceral fat depots.

120 en and estrogen receptor (ER)-alpha suppress visceral fat development through actions in several orga

121 ces in pancreatic, hepatic, subcutaneous and visceral fat distribution compared to NBW participants.

122 has limited potential to accurately estimate visceral fat in a clinical setting.

123 nal subcutaneous fat mass (1650-1850 cm(3)), visceral fat mass (1350-1650 cm(3)), and total body weig

124 e explained exclusively by associations with visceral fat mass (P=0.002), with no association seen be

125 macronutrient and food profiles, may affect visceral fat mass and metabolic syndrome.

126 Abdominal subcutaneous fat, but not visceral fat, area was higher in ELBW survivors compared

127 Increased visceral fat, rather than subcutaneous fat, during the o

128 ntent, aortic pulse wave velocity (PWV), and visceral fat.

129 cantly elevated levels of PDFF and total and visceral fat.

130 the ER stress-induced TRIP-Br2 expression in visceral fat.

131 ER) stress-induced inflammatory responses in visceral fat.

132 , despite HI subjects having marginally more visceral fat.

133 human tissues and ASCs from subcutaneous and visceral fat.

134 al-energy X-ray absorptiometry (DXA)-derived visceral-fat-volume measurements, in a subset of TwinsUK

135 y, vasculopathy, and extensive cutaneous and visceral fibrosis.

136 T: Emotional state is impacted by changes in visceral function, including blood pressure, breathing a

137 Emotional state is impacted by changes in visceral function, including blood pressure, breathing a

138 ons are accompanied by concordant changes in visceral function, including cardiac output, respiration

139 with maraviroc results in a low incidence of visceral GVHD.

140 ion); (2) adiposity (defined by pericardial, visceral, hepatic, and intrathoracic fat); and (3) muscl

141 ed by inflammation, barrier dysfunction, and visceral hypersensitivity (VH).

142 GF mice displayed visceral hypersensitivity accompanied by increases in To

143 Mice with maternal separation developed visceral hypersensitivity and defects in Paneth cells, a

144 n of newborn rats from their mothers induces visceral hypersensitivity and impaired epithelial secret

145 9(flox/flox)-vil-Cre mice also had increased visceral hypersensitivity compared with control litterma

146 BACKGROUND & AIMS: Visceral hypersensitivity is one feature of irritable bo

147 chanisms by which maternal separation causes visceral hypersensitivity or its relationship with defec

148 ers with those of 39 patients with IBS (with visceral hypersensitivity or normal levels of sensitivit

149 ngicide to hypersensitive rats reduced their visceral hypersensitivity to normal levels of sensitivit

150 We investigated whether fungi can cause visceral hypersensitivity using rats exposed to fungicid

151 bjected to water avoidance stress (to induce visceral hypersensitivity), then given fungicide and don

152 combination including motility disturbance, visceral hypersensitivity, altered mucosal and immune fu

153 thecal injection of G-CSF exhibit pronounced visceral hypersensitivity, an effect that is abolished b

154 teric nerve unit may be involved in IBS-like visceral hypersensitivity, and this process is likely in

155 uble beta-glucans or a SYK inhibitor reduced visceral hypersensitivity, compared with controls.

156 sine kinase (SYK), a SYK inhibitor to reduce visceral hypersensitivity, or vehicle (control).

157 ciceptors in a mouse tissue model of chronic visceral hypersensitivity, suggesting the potential of K

158 n studies of rats, we found fungi to promote visceral hypersensitivity, which could be reduced by adm

159 ve intestinal expansion of E coli leading to visceral hypersensitivity.

160 be manipulated for treatment of IBS-related visceral hypersensitivity.

161 ion of E coli during maternal separation and visceral hypersensitivity.

162 omes of patients with IBS and a rat model of visceral hypersensitivity.

163 ult mice with 10(9) commensal E coli induced visceral hypersensitivity.

164 In contrast, the caudal nTS receives general visceral information largely from the vagus nerve.

165 e imaging (fMRI) scanning while performing a visceral interoceptive attention task and a resting-stat

166 s were more frequent in patients treated for visceral involvement than in those treated for skin invo

167 onse to treatment was evaluated for skin and visceral involvement using the ePOST (extra-pulmonary Ph

168 ted for skin involvement and 25 patients for visceral involvement.

169 in humans are ocular larva migrans (OLM) and visceral larva migrans (VLM).

170 Clinical manifestations in canine visceral leishmaniasis (CVL) have not been clearly assoc

171 Visceral leishmaniasis (kala-azar, KA) is the most sever

172 lent, faces the highest burden world-wide of visceral leishmaniasis (VL) and human immunodeficiency v

173 eport a detrimental role of Ly6C(hi) iMOs in visceral leishmaniasis (VL) caused by Leishmania donovan

174 Visceral leishmaniasis (VL) is a potentially fatal paras

175 diseases tegumentary leishmaniasis (TL) and visceral leishmaniasis (VL), is comparatively less well

176 Leishmania donovani causes visceral leishmaniasis (VL), the second most deadly vect

177 ntileishmanial efficacy against experimental visceral leishmaniasis (VL).

178 recently approved for treatment of the fatal visceral leishmaniasis (VL).

179 t infects professional phagocytes and causes visceral leishmaniasis (VL).

180 potential first-in-class drug candidate for visceral leishmaniasis (VL).

181 le utility against the kinetoplastid disease visceral leishmaniasis (VL).

182 ishmania donovani parasites are the cause of visceral leishmaniasis and are transmitted by bites from

183 Patients with active visceral leishmaniasis are important reservoirs in the a

184 y, transmission competence and the impact of visceral leishmaniasis elimination campaigns.Parasitemia

185 is from dogs with clinical manifestations of visceral leishmaniasis in Governador Valadares, an endem

186 hmania donovani, the main causative agent of visceral leishmaniasis in humans, and successfully appli

187 In Brazil, human and canine visceral leishmaniasis is caused by infection with Leish

188 sness of patients for the sand fly vector of visceral leishmaniasis is linked to parasites found in t

189 he relevance of asymptomatic and symptomatic visceral leishmaniasis patients as infection reservoirs.

190 has been considered the main determinant of visceral leishmaniasis transmission.

191 Leishmania donovani, the causative agent of visceral Leishmaniasis, and Leishmania tropica, the caus

192 ania donovani, the main etiological agent of visceral leishmaniasis, and the autophagic machinery of

193 ted in cultures recovered from patients with visceral leishmaniasis.

194 No vaccine exists against visceral leishmaniasis.

195 d immunity and subsequent protection against visceral leishmaniasis.

196 parasites, in a Brazilian city endemic with visceral leishmaniasis.

197 ponses were not limited to injected lesions; visceral lesion decreases were observed in 52% of patien

198 detection of lymph nodes, bone lesions, and visceral lesions was superior to CIM.

199 In conclusion, the visceral mass of M. charruana contains a trypsin-like pr

200 escribes purification of a protease from the visceral mass of the mussel Mytella charruana as well as

201 ted alkaline phosphatase and the presence of visceral metastases were negative predictors and the tot

202 ctionally important mediator of PCa bone and visceral metastases, activating paracrine Shh signaling

203 alutamide use, prior taxane use, presence of visceral metastases, and Eastern Cooperative Oncology Gr

204 cer cells, but not primary mammary tumors or visceral metastases.

205 dormant or progress to cause overt bone and visceral metastases.

206 castration-resistant prostate cancer without visceral metastases.

207 r (and how) lymphangiogenesis contributes to visceral metastasis.

208 SCPs migrate along the visceral motor nerve to the vicinity of the forming adre

209 n structures induced by mst depletion in the visceral muscle as a pathogenic mechanism for VM.

210 arked increase of apoptotic responses in the visceral muscle.

211 demonstrating a critical role of mst in the visceral muscle.

212 Genetic mechanisms for the pathogenesis of visceral myopathy (VM) have been rarely demonstrated.

213 peristalsis syndrome (MMIHS) is a congenital visceral myopathy characterized by severe dilation of th

214 uce intestinal pathology, thereby modulating visceral nociception and IBS symptomatology, and might p

215 ized that a high-FODMAP (HFM) diet increases visceral nociception by inducing dysbiosis and that the

216 el syndrome, are associated with exaggerated visceral nociceptive actions that may involve altered mi

217 a prominent secondary gustatory and general visceral nucleus (SGN/V) located in the isthmic region.

218 ribution to white adipose tissue, leading to visceral obesity at 2 months of age.

219 om the molecular distillation of crude squid visceral oil.

220 the subgroups of RCC patients with regard to visceral or bone metastases or localized disease (p = 0.

221 No case of visceral or chronic GvHD was seen.

222 ia infantum or Leishmania major, which cause visceral or cutaneous leishmaniasis, respectively, elici

223 which have been associated with superficial, visceral, or systemic infections in humans, other mammal

224 uestration of hyperactive neutrophils in the visceral organ.

225 The vagus nerve innervates visceral organs and may contribute to the mediation of g

226 se characterized by fibrosis of the skin and visceral organs and vascular alterations.

227 f MMIHS, confirming that this disease of the visceral organs is heterogeneous with a myopathic origin

228 specification of left-right asymmetry of the visceral organs is precisely regulated.

229 tment, iduronidase activity was increased in visceral organs of MPS-I animals, glycosaminoglycans sto

230 However, noxious sensory signals from visceral organs produce hypersensitive spots on the skin

231 that do not reach conscious sensations from visceral organs to the central nervous system.

232 es and therapeutic effects on the associated visceral organs, which is likely due to the release of e

233 ng with decreased off-target accumulation in visceral organs.

234 somatic afferents in abnormal conditions of visceral organs.

235 r sensory nerves may compromise perfusion of visceral organs.

236 the blood, the lymph nodes, and at times the visceral organs.

237 tment reduces excitability and G-CSF-induced visceral pain in vivo.

238 The perception of visceral pain is a complex process involving the spinal

239 in mice and humans but its significance for visceral pain is unknown.

240 ative behavioural models evoking somatic and visceral pain pathways, we identify the requirement for

241 can prevent the establishment of persistent visceral pain postcolitis.

242 Here we examine the role of NaV 1.7 in visceral pain processing and the development of referred

243 c noxious heat pain, but is not required for visceral pain processing, and advocate that pharmacologi

244 he gut microbiota is required for the normal visceral pain sensation.

245 tic (noxious heat pain threshold) but not in visceral pain signalling.

246 able probiotics have the potential to modify visceral pain.

247 era may be insufficient in targeting chronic visceral pain.

248 ce or correct microbial dysbiosis may impact visceral pain.SIGNIFICANCE STATEMENT Commercially availa

249 The visceral peptidase from farmed giant catfish could be an

250 have slower gastric emptying and heightened visceral perception compared to HC and OB.

251 ry bladder, skeletal muscle, myocardium, and visceral pericardium.

252 ural tags provided weak evidence to rule out visceral pleural invasion (positive LR, 0.38).

253 ra in 141 patients (44 patients [31.2%] with visceral pleural invasion proved by pathologic analysis

254 pleural tags was moderately associated with visceral pleural invasion with the following results: po

255 The visceral protein transthyretin (TTR) is frequently affec

256 Here we report the visceral role of misato (mst) in Drosophila and its impl

257 Interoception, the sensitivity to visceral sensations, plays an important role in homeosta

258 l experiences produces "identity fusion" - a visceral sense of oneness - which in turn can motivate s

259 We used germ-free mice (GF) to assess visceral sensitivity, spinal cord gene expression and pa

260 be determined if gut bacteria play a role in visceral sensitivity.

261 ther poor epithelial resistance or increased visceral sensitivity.

262 reflux exposure, epithelial resistance, and visceral sensitivity.

263 ion and intestinal dysbiosis are involved in visceral sensitivity.

264 his interaction represents a central step in visceral sensitization following colonic inflammation, t

265 factor (G-CSF or Csf-3) as a key mediator of visceral sensitization.

266 action of ANNA-1, in particular anti-HuD, on visceral sensory and enteric neurons, which involves nic

267 the commissural nucleus of Cajal, a general visceral sensory center.

268 s exhibit neural crosstalk by convergence of visceral sensory pathways, and rodent studies demonstrat

269 Unexpectedly, while multiple satiety-related visceral signals converge in insular cortex, chemogeneti

270 These findings reveal how layers of visceral signals operating on distinct timescales conver

271 ed diffusion precludes whole-body imaging at visceral sites.

272 Our data suggest that both visceral smooth and somatic striated myocytes were prese

273 ene preferentially expressed in vascular and visceral smooth muscle cells.

274 the surgeon's action and perception in open visceral surgery by displaying 3D anatomical models clos

275 lization of anatomical structures in complex visceral-surgical interventions.

276 clinical manifestations with tegumentary or visceral symptoms.

277 central connections of the gustatory/general visceral system of the adult zebrafish (Danio rerio) wer

278 ial, dorsal and posterior agranular insular, visceral, temporal association, dorsal and ventral audit

279 fector responses, supporting the presence of visceral thermoreceptors in humans.

280 The present study aimed to determine whether visceral thermoreceptors modify shivering responses to c

281 Visceral thermoreceptors that modify thermoregulatory re

282 KEY POINTS: Visceral thermoreceptors that modify thermoregulatory re

283 , we tested the hypothesis that the ratio of visceral to subcutaneous adipose tissue is associated wi

284 uences encoded by the genomes or salivary or visceral transcriptomes of numerous hard ticks, spanning

285 ase (0 or 1 vs >1), and disease involvement (visceral vs non-visceral).

286 These data indicate that beneficial visceral WAT browning can be engineered by directing vis

287 hysiological consequences of browning murine visceral WAT by selective genetic ablation of Zfp423, a

288 Thermogenic visceral WAT improves cold tolerance and prevents and re

289 ans, expression of TBX15 in subcutaneous and visceral WAT is positively correlated with markers of gl

290 Unlike subcutaneous WAT, visceral WAT is resistant to adopting a protective therm

291 f key thermogenic genes in interscapular and visceral WAT.

292 WAT browning can be engineered by directing visceral white adipocyte precursors to a thermogenic adi

293 ors (Zfp423(l)(oxP/loxP); Wt1-Cre), or adult visceral white adipose precursors (Pdgfrb(rtTA); TRE-Cre

294 yses of body fat, plasma hormone levels, and visceral white adipose tissue DNA methylome and transcri

295 These lead to systemic and visceral white adipose tissue inflammation in addition t

296 was positively related to glucose uptake in visceral white adipose tissue, although glucose uptake i

297 y epigenomic alterations and inflammation in visceral white adipose tissue.

298 ance, indirect calorimetry was performed and visceral white adipose tissues (VWAT) were assessed for

299 d-TC-B12 and TC-(57)CoB12 accumulated in the visceral yolk sac of KO mice where megalin is expressed

300 n was about the same in both WT and KO mouse visceral yolk sac, brain, and spinal column.