ライフサイエンスコーパス: peritoneum

1 g vs 35.62 mg/kg; P = 0.0003 in the parietal peritoneum).

2 e-switched B cells were only detected in the peritoneum.

3 PH B cells preferentially accumulated in the peritoneum.

4 ssure, carry metastatic cells throughout the peritoneum.

5 t low-grade serous carcinoma of the ovary or peritoneum.

6 phil recruitment into inflamed cremaster and peritoneum.

7 ence of local cytokine production within the peritoneum.

8 re is effective in the visceral and parietal peritoneum.

9 ype in dialysis membrane chambers in the rat peritoneum.

10 tant malignant mesothelioma of the pleura or peritoneum.

11 es GRP-induced neutrophil recruitment to the peritoneum.

12 bone marrow and then homed to the spleen and peritoneum.

13 helial cells and probably other cells of the peritoneum.

14 ature splenic NK cells are able to reach the peritoneum.

15 a B1 and follicular B cells persisted in the peritoneum.

16 tion in pro-MMP-9 activation in the inflamed peritoneum.

17 nd chemokine concentrations in the blood and peritoneum.

18 clearance were enhanced within the infected peritoneum.

19 ency results in increased cellularity in the peritoneum.

20 ogens in many organs, including the lung and peritoneum.

21 microbial translocation from the gut to the peritoneum.

22 eria but not inflammatory cells in lungs and peritoneum.

23 immune responses locally at the level of the peritoneum.

24 ness human peritoneum and, in vivo, to mouse peritoneum.

25 pecific recall eosinophil recruitment to the peritoneum.

26 NK cells and killer dendritic cells into the peritoneum.

27 numerous metastases to lymph node, lung, and peritoneum.

28 sms that up-regulate fibrinolysis within the peritoneum.

29 ectable levels observed on B1 B cells in the peritoneum.

30 as did neutrophils infiltrating the inflamed peritoneum.

31 een and increased B1a and B1b B cells in the peritoneum.

32 from the bone marrow and accumulation in the peritoneum.

33 and functional imaging, even through intact peritoneum.

34 apsulated strain, was avirulent in the mouse peritoneum.

35 duced adhesion formation after injury to the peritoneum.

36 earance of apoptotic cells from the inflamed peritoneum.

37 nd no increase of B1a cells in the spleen or peritoneum.

38 2-transfected fibroblasts deposited into the peritoneum.

39 e a potential mechanism for SP action in the peritoneum.

40 rs of the breast, ovary, fallopian tube, and peritoneum.

41 t macrophages in the skin, kidney, heart and peritoneum.

42 d in neutrophils of the peripheral blood and peritoneum.

43 tment and enhancing CXCL10 expression in the peritoneum.

44 colonization and TD Ags translocated to the peritoneum.

45 the low levels of phosphate observed in the peritoneum.

46 side the uterus, most commonly on the pelvic peritoneum.

47 ent to make contact with the entire anatomic peritoneum.

48 . asthma), were particularly elevated in the peritoneum.

49 tiple leiomyomas in the abdominal and pelvic peritoneum.

50 t no impairment in neutrophil recruitment to peritoneum.

51 ytokine and chemokine levels in the infected peritoneum.

52 ascular in the vicinity of the lungs and the peritoneum.

53 essels and VEGF-A-positive cells in fibrotic peritoneum.

54 ymorphonuclear leukocytes instilled into the peritoneum.

55 pithelium than ovarian surface epithelium or peritoneum.

56 V low-grade serous carcinoma of the ovary or peritoneum.

57 cer of the ovary, fallopian tube, or primary peritoneum.

58 penetration indices into meninges, bone, and peritoneum.

59 cer, metastasis is typically confined to the peritoneum.

60 dent models of inflammation in air pouch and peritoneum.

61 aline) was injected between the mesh and the peritoneum.

62 ) characterized by extensive fibrosis of the peritoneum.

63 ns) outside the uterus, most commonly on the peritoneum.

64 cifically recruited from the spleen into the peritoneum.

65 response to thioglycollate injections in the peritoneum.

66 uction, and triggering their exodus from the peritoneum.

67 n to normal mesothelial cells which line the peritoneum.

68 e serosal surface of the small bowel and the peritoneum.

69 rare cancer of the mesothelial cells of the peritoneum.

70 igh-grade serous carcinomas of the ovary and peritoneum.

71 recovery of highly fluorescent GAS from the peritoneum 1 h after challenge.

72 an-elicited neutrophil infiltration into the peritoneum 25-50% and shortened the resolution interval

73 ommon EHD sites included lung (33 patients), peritoneum (32), and portal lymph nodes (14).

74 Bacterial entry into the peritoneum acutely induced macrophage adherence and asso

75 production and neutrophil recruitment to the peritoneum after intraperitoneal administration.

76 these DBP(-/-) mice to recruit cells to the peritoneum after localized thioglycolate injection.

77 We measured KC and MIP-2 in the peritoneum after thioglycollate injection and demonstrat

78 ptimal control of bacterial expansion in the peritoneum also required expression of FV by the macroph

79 h an increased filtration coefficient of the peritoneum and a decreased reflection coefficient to pro

80 ed significant neutrophil migration into the peritoneum and a significant increase in the levels of C

81 rovides 12-24 h of analgesia to the parietal peritoneum and abdominal wall, and are best used combine

82 crophage and microglial recruitment into the peritoneum and brain, respectively, than in wild-type mi

83 cytokines and higher parasite burden in the peritoneum and brain.

84 urthermore, ATF3-null mice lacked MCs in the peritoneum and dermis, showing that the in vitro results

85 Blood monocytes then enter the inflamed peritoneum and develop into new peritoneal macrophages.

86 n 100% of the animals when injected into the peritoneum and developed vascularized tumors in 85% of t

87 ility of the Deltaspx strain to colonize the peritoneum and disseminate in the bloodstream was signif

88 , these Vgamma4+ T cells are retained in the peritoneum and draining mediastinal lymph nodes for a pr

89 are induced during in vivo growth in the rat peritoneum and during in vitro growth in sputum (mucus)

90 ned evidence that macrophages present in the peritoneum and in menses endometrium can contribute to t

91 MCAs) present in ascites fluid adhere to the peritoneum and induce retraction of the peritoneal mesot

92 1 induces fibrosis and angiogenesis in mouse peritoneum and is associated with increased solute trans

93 tor, in F4/80(hi) macrophages in the spleen, peritoneum and kidney.

94 ous HSCs/HPCs were actively recruited to the peritoneum and liver, respectively, in WT but not Ccr2-/

95 is associated with acute fascioliasis in the peritoneum and liver.

96 in vivo neutrophil recruitment to the mouse peritoneum and lung.

97 acrophage-rich portals of entry, such as the peritoneum and lung.

98 Preferential metastatic sites were lungs, peritoneum and lymph nodes.

99 ese SPM-like cells are not restricted to the peritoneum and may help clear apoptotic cells from tissu

100 acrine manner to promote colonization of the peritoneum and neovascularization of developing tumor de

101 ved in solute and water transport across the peritoneum and of the pathobiology of structural and fun

102 Attachment of OvCa cells to peritoneum and omentum represents the first rate-limitin

103 omentum or peritoneum, and in vivo to mouse peritoneum and omentum.

104 IgD(dim)IgM(+) B cell populations in spleen, peritoneum and peripheral blood.

105 her concentrations of CXCL1 and CXCL2 in the peritoneum and plasma compared with those predicted to l

106 ominal fat is abundantly present in both the peritoneum and retroperitoneum.

107 induced 3- and 4-fold more TNF-alpha in the peritoneum and serum, respectively, of db/db mice as com

108 infiltration ( approximately 44%, 6 h) into peritoneum and shortened resolution interval from 4 to 2

109 equencies of latently infected cells in both peritoneum and spleen by 28 days postinfection.

110 spleen to their long-term residence in adult peritoneum and spleen.

111 ection in mice, g-EAR showed gelation in the peritoneum and sustained, local-regional release of EpoB

112 o increased inflammatory infiltrate into the peritoneum and target organs.

113 y made contact with only 40% of the anatomic peritoneum and that this contact area (A(contact)) could

114 an be activated by antigens drained from the peritoneum and the gastrointestinal tract.

115 SU-induced recruitment of neutrophils to the peritoneum and the synovium in wild-type mice, but not i

116 from the urinary tract, and 1 each from the peritoneum and the thorax.

117 e parasite migrated from the gut, across the peritoneum and through the liver to mature in the bile d

118 rophils were able to migrate to the inflamed peritoneum and to phagocytose heat-killed Candida partic

119 mesothelial cells, and full-thickness human peritoneum and, in vivo, to mouse peritoneum.

120 g vs 5.48 mg/kg; P = 0.00001 in the visceral peritoneum, and 66.16 mg/kg vs 35.62 mg/kg; P = 0.0003 i

121 in a 25-75% reduction of cells invading the peritoneum, and a 7-fold increase in LXA(4) identified b

122 lial cells lining the lungs, pericardium and peritoneum, and are often associated with occupational a

123 with primary macrophages derived from lung, peritoneum, and blood but not spleen.

124 responses in the spleen, lungs, bone marrow, peritoneum, and blood using a mouse model of endotoxemia

125 el of metastatic OvCa, full human omentum or peritoneum, and in vivo to mouse peritoneum and omentum.

126 ulation, neutrophil extravasation into lung, peritoneum, and skin wounds was reduced in Tph1(-/-) mic

127 infection, mononuclear cells from the liver, peritoneum, and spleen were isolated.

128 on in specific microenvironments such as the peritoneum, and we would propose other privileged sites,

129 lial cancer of the ovary, fallopian tube, or peritoneum (any stage, grade 2 to 3 if stage I) and meas

130 nally in some mesoderm cells of the visceral peritoneum arranged in an approximately midventral row r

131 We observed NK migration into the infected peritoneum as early as 6 h after vaccinia inoculation.

132 mulation in the interstitium (edema) and the peritoneum (ascites) of nephrotic patients is classicall

133 ncer metastasized to lymph nodes, liver, and peritoneum at a significantly higher rate compared with

134 ntable temperature probe was placed into the peritoneum before asphyxia.

135 activation-involvement of the liver, spleen, peritoneum, bones, and marrow-are frequent.

136 Compartments such as the bladder, peritoneum, brain, eye and skin are often sites of disea

137 poradic EOC commonly remains confined to the peritoneum, BRCA1/2-deficient ovarian cancer frequently

138 t between wild-type MIP-2 and mutants in the peritoneum, but all activity of the mutants is lost in t

139 of M2 macrophages and their accumulation in peritoneum, but not in the liver.

140 C chemokine ligand 12 injection sites in the peritoneum, but not to CXC chemokine ligand 12.

141 ing cells showed increased adhesion to mouse peritoneum, but the overall number of metastatic nodules

142 by delaying the neutrophilic response in the peritoneum by 48 hours and allowing dissemination to var

143 11beta-HSD activity in cells elicited in the peritoneum by a single thioglycolate injection in mice.

144 inhibited recruitment of leukocytes into the peritoneum by specifically activating the A(3)AR.

145 whether host responses originating from the peritoneum can influence PspC expressed by pneumococci i

146 suggest that statins administered within the peritoneum can up-regulate local fibrinolysis, while the

147 nto a massive neutrophil infiltration of the peritoneum capable of neutralizing a septic polymicrobia

148 e used in humans, injection of NBPs into the peritoneum caused recruitment of neutrophils, followed b

149 ragilis and colonic contents escape into the peritoneum, causing abscesses and bacteremia.

150 ease in neutrophil and monocyte entry to the peritoneum compared to scramble mice.

151 y more neutrophils and fewer bacteria in the peritoneum compared with C57BL/6 mice 24 h after CLP.

152 10) concentrations increase in the blood and peritoneum concordant with the peritoneal recruitment of

153 n their ability to migrate into the inflamed peritoneum, confirming that CD13 phosphorylation is rele

154 adhesions derive primarily from the visceral peritoneum, consistent with our clinical experience that

155 macrophages and mesothelial cells lining the peritoneum contain MCP-1, which is released following th

156 cell subsets within lymphoid tissues and the peritoneum could be depleted efficiently in vivo through

157 gly, although NK trafficking to the infected peritoneum depended on G alpha(i) protein-coupled recept

158 Cs), the main source of IL-6 and VEGF in the peritoneum, do not bear the cognate IL-6 receptor and ar

159 giant cells are formed in the inflamed mouse peritoneum during the resolution phase of inflammation,

160 ompared with long-term PD control and uremic peritoneum, EPS peritoneum showed thicker submesothelial

161 ells residing in the bone marrow, blood, and peritoneum, even though cells from the last site had hig

162 -resistant papillary serous carcinoma of the peritoneum experienced a partial response lasting 22 mon

163 Within the peritoneum, F. hepatica antibodies coincided with an int

164 ed to both lymphoid and non-lymphoid organs (peritoneum, fat pads, and lung).

165 data collection process or had done a formal peritoneum-focused review of individual pre-treatment sc

166 110gamma(-/-)) CD8 effector T cells into the peritoneum following i.p. challenge with VV.

167 hibited impaired migration into the inflamed peritoneum following secondary transfer into wild-type r

168 recruitment at a primary site of infection (peritoneum) following lethal murine ehrlichial infection

169 aintained the polymeric nanoparticles in the peritoneum for 1 week, which we had previously shown wou

170 pouch was formed by dissecting the parietal peritoneum from the transversalis fascia of mice.

171 ID1 was increased in peritoneum from women with endometriosis and TGF-beta1 i

172 escents/young adults primarily involving the peritoneum, has a long-term survival of < 20% despite ag

173 ple anatomic sites, including the spleen and peritoneum; however, the contribution of distinct cell t

174 infusion reduced leukocyte migration to the peritoneum in a murine model of thioglycolate-induced pe

175 caused by deposition of AIM at the necrotic peritoneum in AIM (+/+) mice.

176 toneal dialysis are dependent on the area of peritoneum in contact with the dialysis solution, rats w

177 s a result, neutrophils entered the inflamed peritoneum in greater numbers or for a longer duration.

178 id not affect invasion of PDAC into bowel or peritoneum in mice.

179 okines in vitro and increased migration from peritoneum in response to lipopolysaccharide in vivo.

180 Neutrophilic influx into the peritoneum in response to necrotic cells in vivo was als

181 lay no acceleration of infiltration into the peritoneum in spite of elevated L-selectin surface level

182 display the linear dimension of the anatomic peritoneum in the sampling plane.

183 nies by colorectal cancer cells in the mouse peritoneum in vivo.

184 isplay a profound defect in migration to the peritoneum in vivo.

185 nds in vitro, and to an aseptically inflamed peritoneum in vivo.

186 the volume of DSR solution cycled across the peritoneum increased sodium removal and substantially de

187 nstrate increased numbers of B1 cells in the peritoneum, increased serum IgM, IgG, and IgG 2a and sho

188 enovirus to overexpress gremlin in the mouse peritoneum, induced submesothelial thickening, fibrosis,

189 We also found that the peritoneum induces different behavior in mature and imma

190 cavity, usually in the sub-hepatic or retro-peritoneum inferior to the sub-hepatic space.

191 ead of exfoliated tumor cells throughout the peritoneum, initially via the peritoneal fluid, and late

192 ltered immune cell composition of the female peritoneum is controlled by elevated tissue chemokine ex

193 eosinophil recruitment to both the lung and peritoneum is impaired by the lack of CD28, suggesting a

194 s concluded that less than half of the mouse peritoneum is in contact with a large volume of solution

195 These data suggest that the peritoneum is not only home to a new subset of tissue-re

196 Given that adhesion to the abdominal peritoneum is the first step in ovarian cancer dissemina

197 eptic abscesses to the lungs, joints, liver, peritoneum, kidneys, and brain.

198 ade serous carcinoma of the ovary (LGSOC) or peritoneum (LGSPC) is a rare subtype of ovarian or perit

199 of resident and interstitial macrophages of peritoneum, lung, and liver but not spleen.

200 n WT and TFE3(-/-) mice were observed in the peritoneum, lung, and skin.

201 s, such as ear skin and the trachea, tongue, peritoneum, lungs, and bone marrow.

202 ls are rapidly released and recruited to the peritoneum membrane lumen vasculature where they reside

203 tumor invades locally into dermal layers and peritoneum, metastasizes to the lung, and induces a nons

204 s of cancer of the ovary, fallopian tube, or peritoneum (N = 404).

205 tion tubing in the subcutaneous layer (n=3), peritoneum (n=3), aorta (n=3), or carotid artery (n=3).

206 cogen-induced neutrophil emigration into the peritoneum, neutrophil emigration across either the pulm

207 lysis membrane chambers implanted within the peritoneum of a rat.

208 these peptides were co-administered into the peritoneum of baboons with endometriosis, cells in lesio

209 09, decreased neutrophil accumulation in the peritoneum of db/db mice, as well as the accumulation of

210 ed the islets and increased in number at the peritoneum of diabetic but not prediabetic mice.

211 ment blocked neutrophil recruitment into the peritoneum of E-selectin(-/-) mice, but had only a parti

212 trual endometrial tissue introduced into the peritoneum of immunocompetent mice.

213 he heritable disease cystic fibrosis and the peritoneum of individuals undergoing continuous ambulato

214 ly more PspC than did D39 collected from the peritoneum of intraperitoneally (i.p.)-infected mice.

215 vely transferred cells that entered into the peritoneum of mertk-/- mice.

216 ivo neutrophil recruitment into the inflamed peritoneum of mice remains intact in the absence of vinc

217 ioglycollate, neutrophils recruited into the peritoneum of mice were shown to bind more plasminogen t

218 icle-induced pro-inflammatory cascade in the peritoneum of mice.

219 and spleen compared with the bone marrow and peritoneum of normal mice as well as younger mice with l

220 bridoma cells were then transferred into the peritoneum of nude mice to study chronic thyroid stimula

221 resident population of memory T cells in the peritoneum of PD patients and speculate that these cells

222 The peritoneum of puromycin aminonucleoside rats displayed a

223 sion formation was surgically induced in the peritoneum of rats receiving daily doses of the NK-1R an

224 tumor cells were injected directly into the peritoneum of severe combined immunodeficient mice, and

225 aine (according to weight) atomized onto the peritoneum of the right iliac fossa and pelvis, or 20 mL

226 rable neutrophil migration into the inflamed peritoneum of transgenic and wild-type (WT) mice.

227 After 35-days, the peritoneum of tumor-bearing mice with PTX-nanotextiles w

228 and FcepsilonRI double-positive cells in the peritoneum of wild-type (WT) and TFE3 knockout (TFE3(-/-

229 lial cells (HPMCs) recovered from the pelvic peritoneum of women with endometriosis exhibit significa

230 xhibit reduced neutrophil recruitment to the peritoneum on induction of sterile peritonitis and also

231 u expression of endostatin either inside the peritoneum or by the ovarian tumor cells inhibited perit

232 lines as compared to benign tissues (pleura, peritoneum or cysts).

233 end on the involved organs, rarely including peritoneum or digestive tract.

234 a was increased in lesions compared with the peritoneum or eutopic endometrium.

235 uced leukocyte transendothelial migration to peritoneum or lungs was significantly lower in Eng(+/-)

236 not observed following inoculation into the peritoneum or lymph nodes, or after oral ingestion.

237 mice had the phenotype of B-1 B cells in the peritoneum or marginal zone B cells in the spleen, where

238 s and attach preferentially on the abdominal peritoneum or omentum, where the cancer cells revert to

239 adrenal glands, the leukocyte recruitment to peritoneum or the bacterial clearance in liver.

240 i.v. did not prevent dissemination into the peritoneum or to the kidneys, whereas peritoneal adminis

241 re) recruitment of inflammatory cells to the peritoneum, or improve phagocytic cell killing of pathog

242 he spleen, type 2 cytokine production in the peritoneum, or mucus hypersecretion in the gastrointesti

243 , suggesting that monocytes recruited to the peritoneum originate in the spleen.

244 that metastasized to the liver, lung, skin, peritoneum, ovary, and lymph nodes were established.

245 f the drug in both the visceral and parietal peritoneum (P = 0.0058 and P = 0.0044, respectively).

246 3 years) with laparoscopic M1 disease in the peritoneum (P1, adjacent to stomach, 9%; P2, few distant

247 a novel preparation of the isolated parietal peritoneum PD fluid or 3,4-DGE alone, at concentrations

248 We addressed this hypothesis by studying the peritoneum permeability of rats with puromycin aminonucl

249 ants in GP often arise from cells within the peritoneum, presumably pluripotent Mullerian stem cells,

250 ian tube cancers or primary carcinoma of the peritoneum; prior initial therapy with platinum/paclitax

251 man GW39 colon cancer cells into the hamster peritoneum represents a model of tumor spillage that may

252 y osmotic pump (LPS pump) implanted into the peritoneum resulted in sustained, widespread NF-kappaB a

253 g-term PD control and uremic peritoneum, EPS peritoneum showed thicker submesothelial fibrosis, with

254 CCR4(-/-) cells home normally to the peritoneum, showing that they do not have a general defe

255 ng local anesthetic between the mesh and the peritoneum significantly reduces postoperative pain and

256 sessed the E. chaffeensis clearance from the peritoneum, spleen, and liver by C57BL/6J mice using a T

257 senger RNA in macrophages recovered from the peritoneum, spleen, liver and lung, and lowered serum Tn

258 HSCs/HPCs recovered from the peritoneum successfully engrafted into the BM of irradia

259 is at times when macrophages are exiting the peritoneum, suggesting that its proteolytic shedding may

260 stratified by tumors that perforate visceral peritoneum (T4a) versus tumors that invade or are adhere

261 imes more efficient in migrating to inflamed peritoneum than CD8(IL-15) cells.

262 -producing efferocytosing macrophages in the peritoneum that activate invariant natural killer T (iNK

263 n ER stress, IECs communicate signals to the peritoneum that induce a barrier-protective TI IgA respo

264 When transferred directly into the peritoneum, the mature NK cells survive but do not divid

265 are not hyporesponsive; however, within the peritoneum, these B-1 cells are induced to express Lck a

266 0(4) cells in 0.5 ml) were injected into the peritoneum through a midline incision.

267 g fibrinolytic activity in the postoperative peritoneum, thus enabling fibrinous adhesions to persist

268 nd accelerates macrophage clearance from the peritoneum, thus promoting resolution of inflammation an

269 ed a phage display library with female mouse peritoneum tissue and selected phage clones by binding t

270 We find the peritoneum to be rich in glutamate, a glutaminolysis-fue

271 uring the transition of pneumococci from the peritoneum to the blood.

272 ivated beta1 integrin and relocated from the peritoneum to the inflamed skin and intestine upon innat

273 ormal mesothelial cells lining the pleura or peritoneum to the tumor-associated cancer antigen 125 (C

274 amma) and IP-10 production within the septic peritoneum together with local and systemic increases of

275 e faster in vitro, which, in the case of the peritoneum, translates to more rapid in vivo monocyte/ma

276 of Ly6C(hi) inflammatory monocytes into the peritoneum was abolished in type I interferon (IFN-I) re

277 er of inflammatory monocytes in the inflamed peritoneum was associated with a lack of differentiation

278 h VWF-mediated neutrophil recruitment to the peritoneum was described to require the VWF receptor on

279 The absence of PMN in the peritoneum was due in part to lysis of intraperitoneal P

280 hesized that only a fraction of the anatomic peritoneum was in contact with the therapeutic solution

281 Results show that OvCa cell adhesion to the peritoneum was increased under compression.

282 petitively inhibit tumor cell seeding of the peritoneum was investigated.

283 nd that macrophage recruitment into inflamed peritoneum was markedly reduced in the MCP-1-deficient a

284 late-induced neutrophil recruitment into the peritoneum was more severely impaired in P-Rex1(-/-) Vav

285 density of blood vessels per unit length of peritoneum was significantly higher for patients with me

286 Neutrophil trafficking in the peritoneum was similar in all strains after injection of

287 etriosis occurs on organ surfaces facing the peritoneum, we subtracted a phage display library with f

288 colate-induced macrophage recruitment to the peritoneum were indistinguishable between MPhi Sphk dKO

289 stimulate inflammation at the surface of the peritoneum when injected into the abdominal cavity of mi

290 intestine but instead form aggregates in the peritoneum where they produce immunoregulatory molecules

291 atment of large areas such as the pleura and peritoneum, where curative radiation doses cannot be tol

292 ions and agonist-induced neutrophilia in the peritoneum, whereas Galpha(i3) plays a less critical but

293 erthermia enhances diffusion in the visceral peritoneum, whereas high pressure is effective in the vi

294 reatment with neutrophil infiltration to the peritoneum, whereas other investigated cell types remain

295 chaffeensis was cleared in 2 weeks from the peritoneum, whereas the pathogen from tick cells persist

296 eloid-derived suppressor cells (MDSC) in the peritoneum, which expressed functional arginase 1, and p

297 of structural and functional changes in the peritoneum with long-term PD has provided new targets fo

298 the camera to virtually any location in the peritoneum with no working envelope restrictions and the

299 ve markedly decreased PMN infiltrates to the peritoneum with zymosan and altered the dynamics of this

300 IL-6 was also detected in the peritoneum within an hour of infection, prior to the app