ライフサイエンスコーパス: peritoneal

1 presented with metastases (liver [12 of 58], peritoneal [6 of 58], lymph node [15 of 23]).

2 lkine receptor (CX3CR1) in the initiation of peritoneal adhesion important for recolonization of rela

3 Reliable therapeutic options to reduce peritoneal adhesions are scarce.

4 study identifies prevention of postsurgical peritoneal adhesions as a novel and promising field for

5 ays before and seven days after induction of peritoneal adhesions or, alternatively, once during indu

6 Peritoneal adhesions represent a common complication of

7 management of peptic ulcer disease, lysis of peritoneal adhesions, appendectomy, and laparotomy.

8 or, alternatively, once during induction of peritoneal adhesions.

9 the impact of distinct cadherin profiles on peritoneal anchoring of metastatic lesions remains poorl

10 alveolar macrophage phenotype was absent in peritoneal and bone marrow-derived macrophages.

11 0 also promotes the differentiation of mouse peritoneal and human macrophages toward a proinflammator

12 tably, miR-146a expression increased in both peritoneal and intrarenal macrophages in diabetic wild-t

13 d survival during intracellular infection of peritoneal and monocyte-derived macrophages, known to se

14 Similar data from eyelid skin and peritoneal and uterine lavage fluid provide unprecedente

15 und here that although MSKs are activated in peritoneal B cells in response to TLR4 agonists, neither

16 We also show that ATM expression by peritoneal B cells is required to facilitate viral react

17 ing this system we found over a 10-mo-period peritoneal B-1a cell IgM changed, showing the number of

18 demonstrated even in the presence of mature peritoneal B-1a cells, adult bone marrow contributed to

19 r, we found that during long-term infection, peritoneal B-1b, but not related B-1a, B cells display t

20 induced dose-dependent cell death in murine peritoneal B1a cells but NMI did not, suggesting that NM

21 s a caspase-1-dependent pyroptosis in murine peritoneal B1a cells.

22 s third line), and anatomic site (pleural vs peritoneal), by use of an interactive voice or web syste

23 quartile range [IQR], 47-64) years, and mean peritoneal cancer index was 13 (IQR, 7-18).

24 ithelial ovarian, fallopian tube, or primary peritoneal cancer received IMGN853 at 6.0 mg/kg (adjuste

25 n of an invasive ovarian, fallopian tube, or peritoneal cancer.

26 mic intraperitoneal chemotherapy (HIPEC) for peritoneal cancers can be associated with significant co

27 to June 23, 2016, with primary or secondary peritoneal cancers were included.

28 own by immunofluorescence to be expressed in peritoneal capillaries in mice.

29 n in women with ovarian, fallopian tube, and peritoneal carcinoma (OC) causing a greatly increased li

30 gC1qR), is expressed on the cell surface of peritoneal carcinoma cell lines of gastric (MKN-45P), ov

31 that peritoneal tumors in mice and clinical peritoneal carcinoma explants express p32 protein access

32 e rate after cytoreductive surgery (CRS) for peritoneal carcinomatosis (PC) in a tertiary center.

33 the peritoneal cavity - a condition known as peritoneal carcinomatosis (PC).

34 Patient 2 presented with peritoneal carcinomatosis and died after palliative surg

35 in survival in a syngeneic model of ovarian peritoneal carcinomatosis.

36 n of the CSF temporary drainage/externalized peritoneal catheter.

37 strointestinal system as well as pleural and peritoneal cavities but not the brain.

38 ynecological malignancies disseminate in the peritoneal cavity - a condition known as peritoneal carc

39 Mesothelial cells (MCs) line the peritoneal cavity and help define peritoneal response to

40 In the peritoneal cavity and liver, C1q enhancement of type 2 m

41 d on B1 cells outside of the bone marrow and peritoneal cavity and that pathogenic natural IgM titers

42 tigens, particulates, and pathogens from the peritoneal cavity and, depending on the stimuli, promoti

43 al pathogens and affect the cells lining the peritoneal cavity by triggering local inflammation and i

44 eased accumulation of neutrophils within the peritoneal cavity compared with wild-type control mice,

45 s in large microcapsules transplanted in the peritoneal cavity have failed to reverse diabetes in hum

46 , Ly6C(+) monocytes constitutively enter the peritoneal cavity in a CCR2-dependent manner, where they

47 ion of elicited monocytes/macrophages in the peritoneal cavity in response to inflammatory thioglycol

48 flammation in the mouse cremaster muscle and peritoneal cavity led to ICAM-1 expression on intravascu

49 lation was found in spleen, bone marrow, and peritoneal cavity of humanized mice and included distinc

50 6(-)PD-L2(-)MHCII(-)UCP1(+) phenotype in the peritoneal cavity of mice and during the formation of li

51 Fewer DCs also accumulated in the peritoneal cavity of UV-chimeric mice (ie, mice transpla

52 tion of IFN-regulated gene expression in the peritoneal cavity, and an increased production of myeloi

53 bdominal aorta) and catheters (jugular vein, peritoneal cavity, and distal abdominal aorta).

54 GM3 BLT mice and populate the immune system, peritoneal cavity, and peripheral tissues.

55 imarily produced by B1a cells outside of the peritoneal cavity, are integrally involved.

56 ion of polymorphonuclear leukocytes into the peritoneal cavity, as well as abdominal writhings.

57 phaMbeta2 suppressed Mvarphi egress from the peritoneal cavity, decreased the production of anti-infl

58 -reduction by gaining direct access into the peritoneal cavity, enabling elevated drug levels versus

59 cancer cells disseminate readily within the peritoneal cavity, which promotes metastasis, and are of

60 fluids reduce immunological defenses in the peritoneal cavity.

61 in mice when co-injected with CXCL6 into the peritoneal cavity.

62 , resolving, and chronic inflammation in the peritoneal cavity.

63 he cecum and placing it into the recipient's peritoneal cavity.

64 ntenance of IgM(+) B cells in the spleen and peritoneal cavity.

65 +)IgD(lo) B cells in both the spleen and the peritoneal cavity.

66 eater LPS-dependent production of TNF in the peritoneal cavity.

67 presence of small undetected nodules in the peritoneal cavity.

68 extracellular matrix protein fibronectin by peritoneal cell-derived mast cell lysates diminished GBS

69 Our studies showed that BMCMCs and peritoneal cell-derived mast cells produced substantiall

70 row-derived cultured mast cells (BMCMCs) and peritoneal cell-derived mast cells were used as "surroga

71 Intriguingly, following CLP, Nlrp3(-/-) peritoneal cells (primarily neutrophils) demonstrate dec

72 ity to mortality after puberty, and identify peritoneal cells as mediators of pre-pubertal resistance

73 ed and maintained latency in splenocytes and peritoneal cells but did not reactivate efficiently ex v

74 necessary to support viral reactivation from peritoneal cells during long-term infection.

75 dentium Adoptive transfer of macrophage-rich peritoneal cells from EPS-treated mice confers protectio

76 nally, the adoptive transfer of pre-pubertal peritoneal cells improved the survival of post-pubertal

77 Ex-vivo stimulation of PD effluent peritoneal cells increased release of interleukin (IL) 6

78 pubertal recipient mice, while post-pubertal peritoneal cells or vehicle did not.

79 BAP) decreased the refractoriness of LEW rat peritoneal cells to T. gondii infection, resulting in pr

80 ing in proliferation of parasites in LEW rat peritoneal cells which, in turn, led to augmented cell d

81 c cells, mostly macrophages, but not against peritoneal cells, in a perforin/granzyme-dependent manne

82 uced cell influx and TNF-alpha production in peritoneal cells.

83 g ligand of CX3CR1, regulates organ-specific peritoneal colonization.

84 9 of 41 patients in the PD group for pleural-peritoneal communication.

85 ivestock and humans were analysed within the peritoneal compartment to investigate early infection.

86 organ injuries, i.e. polymicrobial sepsis by peritoneal contamination and infection, ischemia-reperfu

87 Levels of peritoneal CTGF expression were increased by CG challeng

88 t significantly reduced both circulating and peritoneal cytokine concentrations.

89 oneal dissemination (n = 22) and/or positive peritoneal cytology (n = 11) without other organ metasta

90 oneal dissemination (n = 22) and/or positive peritoneal cytology (n = 11) without other organ metasta

91 astasis (peritoneal deposits and/or positive peritoneal cytology) have an extremely poor prognosis.

92 astasis (peritoneal deposits and/or positive peritoneal cytology) have an extremely poor prognosis.

93 ediated inflammation as a key contributor in peritoneal damage.

94 PDAC patients with peritoneal metastasis (peritoneal deposits and/or positive peritoneal cytology)

95 PDAC patients with peritoneal metastasis (peritoneal deposits and/or positive peritoneal cytology)

96 The prevalence of patients on automated peritoneal dialysis (APD) is increasing worldwide and ma

97 Many programs have adopted the use of peritoneal dialysis (PD) for fluid management; however,

98 Peritoneal dialysis (PD) is a life-saving form of renal

99 Fungal peritonitis in a patient on peritoneal dialysis (PD) is a refractory injury accompan

100 l may influence the decision for the initial peritoneal dialysis (PD) modality is unknown.

101 Peritoneal dialysis (PD) remains limited by dialysis fai

102 rospectively analyzed 65 patients undergoing peritoneal dialysis (PD) without prior cardiovascular di

103 Technical innovations in peritoneal dialysis (PD), now used widely for the long-t

104 g that limits ultrafiltration in patients on peritoneal dialysis (PD).

105 tients with CKD and is further aggravated by peritoneal dialysis (PD).

106 mains the main cause of technique failure in peritoneal dialysis (PD).

107 se of morbidity and mortality during chronic peritoneal dialysis (PD).

108 Patients with ESRD undergoing peritoneal dialysis develop progressive peritoneal fibro

109 n by peritoneal leukocytes isolated from the peritoneal dialysis effluent (PDE) of noninfected uremic

110 Hemodialysis and peritoneal dialysis were the only forms of treatment ava

111 s in Africa had facilities for hemodialysis, peritoneal dialysis, and kidney transplantation, respect

112 ) countries had facilities for hemodialysis, peritoneal dialysis, and kidney transplantation, respect

113 Hemodialysis, peritoneal dialysis, and transplantation services were f

114 are available from interventional studies in peritoneal dialysis.

115 al infection, but resulted in fibrosis after peritoneal dialysis.

116 eiving hemodialysis than for those receiving peritoneal dialysis.

117 Results Peritoneal disease (PD) pattern, presence of PD in gastr

118 Presence of peritoneal disease in the right upper quadrant (P = .000

119 phragmatic lymphadenopathy (P = .0004), more peritoneal disease sites (P = .0006), and nonvisualizati

120 More peritoneal disease sites (P = .0025) and presence of pou

121 ect survival and prognostically behaves like peritoneal disease.

122 athologically diagnosed with the presence of peritoneal dissemination (n = 22) and/or positive perito

123 athologically diagnosed with the presence of peritoneal dissemination (n = 22) and/or positive perito

124 owed that miR-139-5p overexpression enhanced peritoneal dissemination in a mouse model.

125 se regulates cellular processes required for peritoneal dissemination of cancer cells, one of the pre

126 Development of chemoresistance and peritoneal dissemination of EOC cells are the major reas

127 An animal model of peritoneal dissemination was used to assess the oncogeni

128 and are characterized by TP53 mutations and peritoneal dissemination.

129 technical surgical considerations, including peritoneal drain vs laparotomy.

130 F-alpha were lower at 1 h than at 4 h of the peritoneal equilibration test but the reductions in cyto

131 ronment following antibiotic treatment for a peritoneal Escherichia coli infection.

132 g cells adhere avidly to both intact ex vivo peritoneal explants and three-dimensional collagen gels.

133 Low concentrations of peritoneal extracellular glutamine during PD may contrib

134 y macrophages in vitro and reactivation from peritoneal exudate cells in vivo.

135 The peritoneal exudate of pristane-treated mice contained ma

136 and in vitro assays applying macrophages and peritoneal fibroblasts indicated that this effect was co

137 ages, impaired recruitment and activation of peritoneal fibroblasts, mitigated epithelial-mesenchymal

138 Peritoneal fibrosis (PF) is a serious complication in va

139 are important regulators, but their roles in peritoneal fibrosis are largely unknown.

140 , IL-17 blockade in cd69(-/-) mice decreased peritoneal fibrosis to the WT levels, and mixed bone mar

141 oing peritoneal dialysis develop progressive peritoneal fibrosis, which may lead to technique failure

142 rity ex vivo and in vivo in a mouse model of peritoneal fibrosis.

143 parent activity of C5L2 in infection-induced peritoneal fibrosis.

144 dWAT expansion and protection from skin and peritoneal fibrosis.

145 ive the stresses of anchorage-free growth in peritoneal fluid and ascites, and to colonize remote sit

146 amount of parasite in the brain, spleen, and peritoneal fluid and reducing brain cysts by >85%.

147 tations (median mutant fraction 1/13,139) in peritoneal fluid from nearly all patients with and witho

148 etect extremely rare cancer cells present in peritoneal fluid from women with high-grade serous ovari

149 Proteomic analysis of the peritoneal fluid identified infection-related proteins,

150 Although plasma and peritoneal fluid levels of IL-33 have been associated wi

151 TP53 mutation was detected in 94% (16/17) of peritoneal fluid samples from women with HGSOC (frequenc

152 x sequencing to analyze TP53 mutations in 17 peritoneal fluid samples from women with HGSOC and 20 fr

153 ted arachidonic acid (AA) derivatives in the peritoneal fluid.

154 tion and vascular proliferation and restored peritoneal function in mouse models of peritonitis, even

155 Dissection of the right vagus decreased peritoneal group 3 innate lymphoid cell (ILC3) numbers a

156 Clinical studies suggest that intra-peritoneal (i.p.) chemotherapy effectively treats residu

157 um cytokines and differential recruitment of peritoneal immune cells.

158 hen applied this assay to test the impact on peritoneal immune-competence of PD fluid supplementation

159 called milky spots (MSs), that contribute to peritoneal immunity by collecting antigens, particulates

160 organization, and function of the omentum in peritoneal immunity.

161 .01), but not with gross residual disease or peritoneal implants.

162 The peritoneal infection model using Porphyromonas gingivali

163 Activation of NR1D1 reduced the severity of peritoneal inflammation and fulminant hepatitis in mice.

164 ruption of Nr1d1 developed more-severe acute peritoneal inflammation and fulminant hepatitis than con

165 In vivo, induction of peritoneal inflammation in wild-type and IL-6-deficient

166 e release of multiple chemokines after acute peritoneal inflammation initiated by a single applicatio

167 hey effectively recruit T cells in vivo in a peritoneal inflammation model.

168 igation and puncture, a model used to induce peritoneal inflammation through infection.

169 ional fibrin matrix and during resolution of peritoneal inflammation, whereas migration of CD11b(-/-)

170 ccelerated resolution of both subretinal and peritoneal inflammation, with implications for the treat

171 intraperitoneal injections of LPS to induce peritoneal inflammation; plasma samples were isolated an

172 Uremia contributed partially to peritoneal inflammatory and fibrotic responses.

173 It has not been well studied in acute peritoneal inflammatory conditions.

174 fibers showed significant alterations of the peritoneal inflammatory response, including significantl

175 rated inflammatory response to cutaneous and peritoneal inflammatory stimuli.

176 Following intra-peritoneal injection of endotoxin, pre-pubertal mice sho

177 Peritoneal injection of RNA or miR-146a led to an increa

178 the efficacy of common methods, such as the peritoneal injections of caerulein, L-arginine, the retr

179 t in piglets first sensitized by three intra-peritoneal injections of peanut protein extract (PPE) wi

180 ]), lung involvement (10 [16.7%]), localized peritoneal involvement (4 [6.7%]), or other (8 [13.3%])

181 The pattern of metastasis and in particular, peritoneal involvement, results in prognostic heterogene

182 FAST, invasive procedures such as diagnostic peritoneal lavage and exploratory laparotomy were common

183 levels of proinflammatory cytokines in both peritoneal lavage and serum.

184 ignificant increase in the levels of CCL4 in peritoneal lavage fluid.

185 otic and inflammatory mediator production by peritoneal leukocytes isolated from the peritoneal dialy

186 Vagotomy resulted in an inflammatory peritoneal lipid mediator profile characterized by reduc

187 n injury in two mouse models of sepsis-intra-peritoneal lipopolysaccharide and cecal ligation and pun

188 C counteracts the LPS effect using a PMJ2-PC peritoneal macrophage cell line.

189 ide increased liver injury and the levels of peritoneal macrophage cytokines, including IL-1beta, in

190 We examined the role of iPLA2beta in peritoneal macrophage immune function by comparing wild

191 ulated platelets also significantly enhanced peritoneal macrophage phagocytosis of both methicillin-r

192 ate lymphoid cell (ILC3) numbers and altered peritoneal macrophage responses.

193 bolism were evaluated in nonactivated murine peritoneal macrophages (MPhi0) and macrophages stimulate

194 or M2 activation of RAW264.7 macrophages and peritoneal macrophages (PM) on subsequent HSV-1 infectio

195 nt with the expression of these receptors in peritoneal macrophages (TLR2/4, C5aR) and mesothelial ce

196 We collected naive peritoneal macrophages and plasma, at multiple times of

197 cluding previously underappreciated roles of peritoneal macrophages and platelets.

198 ne macrophages, such as primary alveolar and peritoneal macrophages and the macrophage cell line RAW2

199 files between bone marrow-derived (BMDM) and peritoneal macrophages differed drastically.

200 c submucosa of Gal3-deficient mice.In vitro, peritoneal macrophages from Gal3-deficient mice were ine

201 Peritoneal macrophages from M-JAK2(-/-) mice and Jak2 kn

202 Depletion of resident peritoneal macrophages prior to, or concomitant injectio

203 more, C1q-deficient pristane-primed resident peritoneal macrophages secreted significantly less CCL3,

204 e, investigation of the activation status of peritoneal macrophages showed that the expression of gen

205 creased phosphorylation of ERK1/2 and Akt in peritoneal macrophages stimulated ex vivo by LPS.

206 In Candida albicans-infected resident peritoneal macrophages, activation of group IVA cytosoli

207 ed in RAW264 macrophage-like cells or murine peritoneal macrophages, and their influence on LPS-induc

208 st (IL-1Ra) secretion in LPS-activated mouse peritoneal macrophages, and this response was regulated

209 PEGs) stimulate potent cytokine responses in peritoneal macrophages, despite not being internalized.

210 In peritoneal macrophages, expression of NLRP3 and activati

211 rain mononuclear cells, blood monocytes, and peritoneal macrophages, suggesting that cell surface CD3

212 on causes a decrease in the thiol content of peritoneal macrophages, which can influence IL-12 produc

213 east tumors to identify peptides that target peritoneal macrophages.

214 (keyhole limpet hemocyanin), on cultures of peritoneal macrophages.

215 ies in patients with unresectable pleural or peritoneal malignant mesothelioma who had progressed aft

216 Co-culture of Leishmania with Peritoneal Mast Cells (PMCs) from BALB/c mice and Rat Ba

217 ization and the expression of FcepsilonRI on peritoneal MCs were quantitated.

218 rammed cell death 4 protein was decreased in peritoneal membrane biopsy specimens from PD patients co

219 Increased miR-21 was found in peritoneal membrane biopsy specimens from PD patients co

220 f the NLRP3 inflammasome and IL-1beta in the peritoneal membrane during acute peritonitis have not be

221 ) remains limited by dialysis failure due to peritoneal membrane fibrosis driven by inflammation caus

222 cing tissue remodeling with consequences for peritoneal membrane integrity.

223 al growth factor (VEGF) is implicated in the peritoneal membrane remodeling that limits ultrafiltrati

224 During peritonitis, the peritoneal membrane undergoes structural and functional

225 e beta1-fragment with the mesothelium of the peritoneal membrane via a biomaterial abrogates the rele

226 as an important effector of fibrosis in the peritoneal membrane, and a promising biomarker in the di

227 d peritonitis led to IL-1beta release in the peritoneal membrane.

228 IL-6 trans-signaling and angiogenesis in the peritoneal membrane.

229 Human peritoneal mesothelial cells (HPMCs), the main source of

230 vitro studies using NIH 3T3 fibroblasts and peritoneal mesothelial cells (PMCs) showed that CTGF blo

231 MCAs were also shown to efficiently rupture peritoneal mesothelial cells, exposing the submesothelia

232 the peritoneum and induce retraction of the peritoneal mesothelial monolayer prior to invasion of th

233 eural mesothelioma or RECIST version 1.1 for peritoneal mesothelioma.

234 Interaction of these MCAs with peritoneal mesothelium disrupts mesothelial integrity, e

235 h isolated peritoneal metastases, those with peritoneal metastases and two or more additional sites o

236 rence because of widespread dissemination of peritoneal metastases at diagnosis.

237 Compared with patients with isolated peritoneal metastases, those with peritoneal metastases

238 , p=0.37) was similar to those with isolated peritoneal metastases.

239 urvival between populations with and without peritoneal metastases.

240 e local excision, whole-organ resection, and peritoneal metastases.

241 PDAC patients with peritoneal metastasis (peritoneal deposits and/or positi

242 PDAC patients with peritoneal metastasis (peritoneal deposits and/or positi

243 erapy, about 60% of patients will re-develop peritoneal metastasis and about 50% will relapse with ch

244 parenchymal invasion (LPI) from perihepatic peritoneal metastasis and hematogenous liver metastases.

245 and the development of advanced and relapsed peritoneal metastasis and its impact on patients' outcom

246 Mechanisms supporting advanced and relapsed peritoneal metastasis are largely unknown, precluding de

247 he fractalkine axis in advanced and relapsed peritoneal metastasis in epithelial ovarian carcinoma.

248 A within tumor microenvironment could enable peritoneal metastasis of ovarian cancer via induction of

249 dvanced, relapsed and chemotherapy-resistant peritoneal metastasis, which is refractory to the curren

250 c ductal adenocarcinoma (PDAC) patients with peritoneal metastasis.

251 ion important for recolonization of relapsed peritoneal metastasis.

252 ity in chemotherapy-naive PDAC patients with peritoneal metastasis.

253 2%] of 289), compared with patients with non-peritoneal metastatic colorectal cancer (194 [9%] of 223

254 Patients with peritoneal metastatic colorectal cancer have significant

255 04, 95% CI 0.86-1.25, p=0.69) and those with peritoneal metastatic colorectal cancer plus one other s

256 18%] of 44 patients with available data) and peritoneal metastatic colorectal cancer with other sites

257 els to assess the prognostic associations of peritoneal metastatic colorectal cancer with overall sur

258 peritoneal sites than in those with isolated peritoneal metastatic colorectal cancer.

259 Experimental therapy of mice bearing peritoneal MKN-45P xenografts and CT-26 syngeneic tumors

260 t of highly phagocytic MPhi resembling small peritoneal MPhi (SPM) that expressed CD138(+) and the sc

261 MO rapidly depleted resident (Tim4(+)) large peritoneal MPhi.

262 Loading with oxLDL did not induce peritoneal Mvarphi apoptosis or modulate basal-level exp

263 y gene expression in thioglycollate-elicited peritoneal Mvarphis, bone marrow-derived Mvarphis and de

264 bited progressive inflammation and sustained peritoneal necrosis tissue on day 28 after the disease i

265 njected with miR-133a or miR-146a had marked peritoneal neutrophil and monocyte migration, which was

266 tic ablation of EC Notch signaling inhibited peritoneal neutrophil infiltration in an ovarian carcino

267 influence in vivo function, we characterized peritoneal neutrophil recruitment of a trapped monomer a

268 We used a mouse model of peritoneal neutrophilic inflammation to determine if Ang

269 ma interferon (IFN-gamma)-stimulated primary peritoneal neutrophils (PPNs) killed chlamydiae in vitro

270 d also distinguishes between ventricular and peritoneal occlusions.

271 patients with mutated BRAF in patients with peritoneal-only (eight [18%] of 44 patients with availab

272 grade endometrioid cancer, including primary peritoneal or fallopian tube cancer.

273 Monocytes first entered peritoneal or pleural cavities to become MHC II(+) cells

274 ble or evaluable epithelial ovarian, primary peritoneal, or fallopian tube cancer, and a clinical com

275 rade serous or endometrioid ovarian, primary peritoneal, or fallopian tube carcinoma, had received at

276 Small tumors attached to peritoneal organs, with vascularity ranging from 2% to 1

277 murine sepsis was associated with increased peritoneal (p = 0.037), systemic (p = 0.019), and bronch

278 s leptin and interleukin 1beta and decreased peritoneal proinflammatory CD86 immunoreactive macrophag

279 al scores, 2 wk after pristane injection the peritoneal recruitment of CD11b(+) Ly6C(high) inflammato

280 In addition, we find that peritoneal-resident macrophage mitochondria are recruite

281 , a glutaminolysis-fuel that is exploited by peritoneal-resident macrophages to maintain respiratory

282 ) line the peritoneal cavity and help define peritoneal response to treatment-associated injury, a ma

283 imulating a supine infant with a ventricular-peritoneal shunt and controlled occlusions.

284 in reduction of metastatic burden at several peritoneal sites commonly colonized by advanced and rela

285 ll survival of patients with two of more non-peritoneal sites of metastasis (adjusted HR 1.04, 95% CI

286 03) was better in patients with isolated non-peritoneal sites than in those with isolated peritoneal

287 led to an increase in cfB expression in the peritoneal space that was attenuated in MyD88-knockout o

288 nd the retention of the nanoparticles in the peritoneal space.

289 We obtained peritoneal specimens from children with stage 5 CKD at t

290 other implants, presence and distribution of peritoneal spread, presence and size of pleural effusion

291 elioma at an earlier age that was more often peritoneal than pleural (five of nine) and exhibited imp

292 Expression analyses of cytokines in peritoneal tissue and fluid and in vitro assays applying

293 These findings reveal the influence of peritoneal TLR2 and TLR4 on PD-associated fibrosis and d

294 n inflammation, we assessed the potential of peritoneal TLR2, TLR4 and C5a receptors, C5aR and C5L2,

295 ells significantly reduced proliferation and peritoneal tumor formation in athymic nude mice.

296 d tumor cell proliferation, angiogenesis and peritoneal tumor growth in immunodeficient mice.

297 sulted in significant reduction of weight of peritoneal tumors and significant decrease in the number

298 (SKOV-3), and colon (CT-26) origin, and that peritoneal tumors in mice and clinical peritoneal carcin

299 KDM4B also regulates seeding and growth of peritoneal tumors in vivo, where its expression correspo

300 The system also facilitates the detection of peritoneal tumors with high specificity upon intraperito