ライフサイエンスコーパス: pleural

1 s; 75 men, 25 women) suspected of having MPM pleural abnormalities underwent positron emission tomogr

2 ofusion, and presence of large opacities and pleural abnormalities.

3 air leakage occurred after the liberation of pleural adhesions.

4 air leakage occurred after the liberation of pleural adhesions.

5 Of 100 patients, 33 had benign pleural alterations, and 67 had malignant pleural diseas

6 (TGF-alpha), established by the presence of pleural and peribronchial fibrosis and impaired lung mec

7 eding the gastrointestinal system as well as pleural and peritoneal cavities but not the brain.

8 In contrast to recent studies in the pleural and peritoneal cavities, the proliferation of re

9 the pleural cavity, and heightened levels of pleural and serum proinflammatory cytokines and chemokin

10 ) fluid; sputum and lung tissue samples; and pleural and spinal fluids.

11 ent infection, resulting in overt pulmonary, pleural, and extrapulmonary tuberculosis.

12 e by FALC stromal cells, ILC2 activation and pleural B-cell activation in FALCs, resulting in local a

13 IL-33 produced by FALC stroma is crucial for pleural B1-cell activation and local IgM secretion.

14 rast, CCR5(-/-) mice survived and controlled pleural BCG infection as wild-type control mice.

15 drainage of pleural fluid via an indwelling pleural catheter led to a higher rate of autopleurodesis

16 procedure, and pleural procedure (indwelling pleural catheter vs other).

17 age; n = 76) of pleural fluid via a tunneled pleural catheter.

18 Indwelling pleural catheters allow patients to drain pleural fluid

19 is following the placement of the indwelling pleural catheters.

20 tes the pleuroperitoneal folds isolating the pleural cavities before the migration of the somitic myo

21 od monocytes recruited to the peritoneal and pleural cavities constitutively, starting after birth, w

22 Monocytes first entered peritoneal or pleural cavities to become MHC II(+) cells that up-regul

23 -derived cells accumulated in peritoneal and pleural cavities, but CD11c(+) CD226(+) macrophages were

24 uced recruitment of mononuclear cells to the pleural cavity and migration of macrophages at transwell

25 hysiological cues that activate FALCs in the pleural cavity and more generally the mechanisms control

26 Plasmin injection into the pleural cavity of BALB/c mice induced a time-dependent i

27 Plg/Pla injection into the pleural cavity of BALB/c mice induced a time-dependent i

28 r long CNTs or long asbestos fibers into the pleural cavity of mice induces mesothelioma that exhibit

29 lung inflammation, that inflammation of the pleural cavity rapidly activates mediastinal and pericar

30 An injection of carrageenan (CAR) into the pleural cavity triggered an acute inflammatory response,

31 y cell recruitment and bacterial load in the pleural cavity, and heightened levels of pleural and ser

32 d PAR2 (F2RL1) generated large tumors in the pleural cavity.

33 e of various human cancers metastatic to the pleural cavity.

34 y located in the lung with a small amount of pleural contact.

35 anastomotic leak with limited mediastinal or pleural contamination.

36 iotics treatment, which is dependent on both pleural cytokine environment and direct modulatory effec

37 gn pleural alterations, and 67 had malignant pleural diseases (MPDs); 57 of 67 had MPM.

38 Pleural disseminated, mutant KRAS bearing tumour cells u

39 ns was associated with prolonged post-Fontan pleural drainage (HR, 4.0; P<0.001) and hypoplastic left

40 ive when performed along with mediastinal or pleural drainage.

41 PCs (13.2% vs 40.5%, P < 0.001), symptomatic pleural effusion (11.6% vs 26.4%, P = 0.003), pleural ef

42 (20%), intrathoracic lymphadenopathy (16%), pleural effusion (12%), reticular infiltration (4%), and

43 opathy (23%), mass-like consolidation (17%), pleural effusion (8.6%), and honey combing (5.7%).

44 Chylous pleural effusion (chylothorax) frequently accompanies ly

45 -2.2% to 17.6%) or postoperative pericardial/pleural effusion (colchicine, 103 patients [57.2%]; plac

46 Malignant pleural effusion (MPE) is the lethal consequence of vari

47 us pleural effusion (TPE, n = 50), malignant pleural effusion (MPE, n = 41), other cases including pn

48 e included patients with pneumonia (n = 28), pleural effusion (n = 13), pleural empyema (n = 4), lung

49 none), dyspnoea (six [2%] vs one [1%]), and pleural effusion (six [2%] vs none).

50 cancer were thrombocytopenia (eight [11%]), pleural effusion (six [8%]), and increased lipase (five

51 We enrolled 91 cases, including tuberculous pleural effusion (TPE, n = 50), malignant pleural effusi

52 ome features was strong (eg, alpha = .78 for pleural effusion and ascites) but was lower for others (

53 ded the use of ultrasonography for ruling-in pleural effusion and assisting its drainage, ascites dra

54 adiologically as interstitial pneumonia with pleural effusion and clinically as hypoxemic respiratory

55 CAP with pleural effusion and documented pneumococcal CAP were di

56 unrelated to alectinib: acute renal failure; pleural effusion and pericardial effusion; and brain met

57 urs in mouse models of malignant lung cancer pleural effusion and spontaneous colon cancer metastasis

58 ion, but 1 patient developed pericardial and pleural effusion attributed to pericardial instrumentati

59 rom 41.3% to 29.7% (P < .001), the number of pleural effusion cases decreased by 53% (167 to 79; P <

60 to improve overall survival in patients with pleural effusion due to malignant pleural mesothelioma,

61 tasis have a history of asbestos exposure or pleural effusion due to various causes.

62 n 480 (39.5%) patients including symptomatic pleural effusion in 366 (30.1%) patients, respiratory in

63 Pleural effusion is a frequent finding in patients with

64 reasing periaortic hematoma, and hemorrhagic pleural effusion on imaging identify patients with compl

65 Methods Patients with NSCLC (stage IIIB with pleural effusion or stage IV according to American Joint

66 leural effusion (11.6% vs 26.4%, P = 0.003), pleural effusion requiring drainage (1.7% vs 9.9%, P = 0

67 HH is a transudative pleural effusion seen in 5%-10% of cirrhosis patients, i

68 Pleural effusion volume was determined on each CT scan s

69 d causing medium lobe atelectasis; bilateral pleural effusion was also present.

70 ents identified in either treatment arm, and pleural effusion was the only drug-related, nonhematolog

71 First occurrences of pleural effusion were reported with dasatinib, with the

72 er radiologic findings (multiple nodules and pleural effusion) were less frequent, but appeared later

73 primary tumor, pleural metastases, malignant pleural effusion, and ascites obtained during disease pr

74 arch for thickening of the gallbladder wall, pleural effusion, and ascites.

75 ata suggest a strong impact of PCV13 on CAP, pleural effusion, and documented pneumococcal pneumonia,

76 Reported events included seizure, pleural effusion, and lymphocytopenia.

77 that increased gall bladder wall thickness, pleural effusion, ascites, hepatomegaly, and splenomegal

78 Among patients with malignant pleural effusion, daily drainage of pleural fluid via an

79 ever, higher morbidity of tachypnea/dyspnea, pleural effusion, diarrhea, hepatosplenomegaly, consciou

80 For treatment of malignant pleural effusion, nonsteroidal anti-inflammatory drugs (

81 of confirmed or suspected mesothelioma with pleural effusion, recruited from 12 hospitals in the UK.

82 other signs (ie, halo sign, hypodense sign, pleural effusion, reversed halo sign) is unknown.

83 t upper lobe mass along with a moderate-size pleural effusion.

84 owed mild pulmonary edema with a small right pleural effusion.

85 rentially diagnose tuberculous and malignant pleural effusion.

86 aphy showed an enlarged heart with bilateral pleural effusion.

87 ractory MPP children or in MPP children with pleural effusion.

88 ostoperative AF or postoperative pericardial/pleural effusion.

89 nts were postoperative AF and pericardial or pleural effusion.

90 esis is performed to identify the cause of a pleural effusion.

91 anulomas as well as ascites and a left-sided pleural effusion.

92 nical characters, such as refractoriness and pleural effusion.

93 quantified MCs in human and murine malignant pleural effusions (MPEs) and evaluated the fate and func

94 Two patients, including one with large pleural effusions and another with ventricular tachycard

95 n of peritoneal spread, presence and size of pleural effusions and ascites, lymphadenopathy, and dist

96 tered to improve the drainage of complicated pleural effusions and empyemas and it is the most effect

97 gnificantly post antibiotic treatment in the pleural effusions and pleural macrophages up-regulated m

98 )CD16(-) NK cells isolated from inflammatory pleural effusions display a potent regulatory activity.

99 d we also detected CXCL12-gamma in malignant pleural effusions from patients with breast cancer.

100 values can help in differentiating exudative pleural effusions from transudative pleural effusions.

101 RATIONALE: Patients with malignant pleural effusions have significant dyspnea and shortened

102 L/One hundred and twenty eight patients with pleural effusions on thoracic CT who underwent thoracent

103 cantly (P<0.0001) associated with pneumonia, pleural effusions requiring drainage, and maximum postop

104 Pleural effusions were classified as exudates or transud

105 The incidence of pleural effusions were not significantly different betwe

106 Thirty three (26%) of the 128 pleural effusions were transudates and 95 (74%) were exu

107 tomography (CT) findings for characterizing pleural effusions with the use of attenuation values.

108 ntestinal and/or pulmonary lymphangiectasia, pleural effusions, chylothoraces and/or pericardial effu

109 xudative pleural effusions from transudative pleural effusions.

110 thoracic notum as well as the already known pleural elements of the arthropodan leg.

111 eumonia (n = 28), pleural effusion (n = 13), pleural empyema (n = 4), lung abscess (n = 7), pericardi

112 leural tag with soft tissue component at the pleural end; and type 3, one or more soft tissue cord-li

113 tures that were evaluated for distinguishing pleural exudates from transudates included pleural nodul

114 ased numbers of apoptotic neutrophils in the pleural exudates, inhibition of elastase, and modulation

115 the most accurate diagnostic indicators for pleural exudates.

116 ion and increased levels of CCL2 and IL-6 in pleural exudates.

117 d target for amelioration of empyema-related pleural fibrosis and provide a strong rationale for furt

118 In pleural fibrosis excess collagen deposition results in p

119 an resolve with restrictive lung disease and pleural fibrosis.

120 lier age that was more often peritoneal than pleural (five of nine) and exhibited improved long-term

121 tum (n = 3), endobronchial washings (n = 3), pleural fluid (n = 1), and the Wesley Hospital WDS (n =

122 71), bronchoalveolar lavage fluid (n = 152), pleural fluid (n = 76), cerebral spinal fluid (CSF; n =

123 on in pleural tumor cells, thereby fostering pleural fluid accumulation and tumor growth.

124 the diagnostic value of IL-31 levels in the pleural fluid and plasma to differentially diagnose tube

125 the detection of M. tuberculosis in sputum, pleural fluid and urine samples.

126 recovery of Mycobacterium tuberculosis from pleural fluid are not statistically different than those

127 ng pleural catheters allow patients to drain pleural fluid at home and can lead to autopleurodesis.

128 /L (LR, 18; 95% CI, 6.8-46), or the ratio of pleural fluid cholesterol to serum cholesterol was great

129 sterol and pleural fluid LDH levels, and the pleural fluid cholesterol-to-serum ratio are the most ac

130 dentified from lung aspirate culture or PCR, pleural fluid culture or PCR, blood culture, and immunof

131 e blood culture or positive lung aspirate or pleural fluid culture or polymerase chain reaction [PCR]

132 Pleural fluid cytology was positive for adenocarcinoma.

133 current standard every other day drainage of pleural fluid in achieving autopleurodesis.

134 o of pleural fluid LDH to serum LDH >0.6, or pleural fluid LDH >two-thirds the upper limit of normal

135 Light's criteria, cholesterol and pleural fluid LDH levels, and the pleural fluid choleste

136 id protein to serum protein >0.5, a ratio of pleural fluid LDH to serum LDH >0.6, or pleural fluid LD

137 al within 15 to 20 min and worked well using pleural fluid obtained directly from CCPP-positive anima

138 es holarctica was isolated from the blood or pleural fluid of 10 individuals from July to September 2

139 appaBalpha(+) populations in whole blood and pleural fluid of a mouse model of lung inflammation.

140 likely when all Light's criteria (a ratio of pleural fluid protein to serum protein >0.5, a ratio of

141 ainage (every other day drainage; n = 76) of pleural fluid via a tunneled pleural catheter.

142 alignant pleural effusion, daily drainage of pleural fluid via an indwelling pleural catheter led to

143 date was most accurate if cholesterol in the pleural fluid was greater than 55 mg/dL (LR range, 7.1-2

144 Ultimately, the combination of pleural fluid with the plasma tuberculosis-specific IL-3

145 = 41), other cases including pneumonia with pleural fluid, pulmonary tuberculosis and healthy people

146 A immunoreactivity in the pedal and cerebral-pleural ganglia across species.

147 gamation of elements from both the notal and pleural hypotheses.

148 d, pneumonia-related effusion to a confirmed pleural infection have been well described in the scient

149 cterium bovis bacillus Calmette-Guerin (BCG) pleural infection in a murine model.

150 ies examining the microbiological profile of pleural infection inform antibiotic choice and can help

151 BCG-induced pleural infection was uncontrolled and progressive in ab

152 nical indices to predict which patients with pleural infection will have a poor outcome, as well as i

153 Data suggests that not all pleural infections can be related to lung parenchymal in

154 s MPEs did not form in mice lacking MCs, and pleural infusion of MCs with MPE-incompetent cells promo

155 Pleural injection of Plg/Pla also increased M2 markers (

156 gen activator and plasmin) are elaborated in pleural injury and strongly induce MesoMT in vitro.

157 nistration of 9ING41, after the induction of pleural injury, attenuated injury progression and improv

158 3beta signaling in the control of MesoMT and pleural injury.

159 incidence of PTM within 7 cm of the site of pleural intervention within 12 months from randomisation

160 Gy in three fractions within 42 days of the pleural intervention) or deferred radiotherapy (same dos

161 months (failure defined as need for further pleural intervention; noninferiority comparison; margin,

162 en mesothelioma who had undergone large-bore pleural interventions in the 35 days prior to recruitmen

163 (P < .01), TNM stage (P < .01), and visceral pleural invasion (P < .01).

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

165 nimal increase in the likelihood of visceral pleural invasion (positive LR, 1.68).

166 the accuracy of early diagnosis of visceral pleural invasion by NSCLC that does not abut the pleura.

167 patients (44 patients [31.2%] with visceral pleural invasion proved by pathologic analysis and 97 pa

168 Older age (P = 0.039), visceral pleural invasion to the surface (PL2) (P = 0.009), and h

169 In the absence of pleural tags, no pleural invasion was found.

170 tags was moderately associated with visceral pleural invasion with the following results: positive LR

171 gic analysis and 97 patients [68.8%] without pleural invasion) was conducted at a single tertiary cen

172 Measurement of cytokines from the pleural lavage showed that mice implanted with MPM cells

173 status of this key tumor suppressor gene in pleural lesions preceding mesothelioma.

174 ge, 65 years +/- 11 [standard deviation]; 86 pleural lesions; 187 pulmonary lesions) had pleural orig

175 Pleural loculation affects about 30,000 patients annuall

176 Thus, MHC II(+) resident peritoneal and pleural macrophages are continuously replenished by bloo

177 Here, we examined whether and how pleural macrophages change in phenotype, transcription a

178 ic genes could be used to study the roles of pleural macrophages in the pathogenesis of tuberculous p

179 nes was modulated directly by antibiotics in pleural macrophages in vitro.

180 Pleural macrophages play critical roles in pathogenesis

181 Our results conclude that pleural macrophages polarize from M1-like to M2-like phe

182 iotic treatment in the pleural effusions and pleural macrophages up-regulated markers characteristic

183 d 230 treatment-specific responsive genes in pleural macrophages.

184 s necessary for the morphologic integrity of pleural membrane and that loss of Wt1 contributes to IPF

185 in vascular endothelium (eg, lymphatics) and pleural mesothelia.

186 ming growth factor-beta1 (TGF-beta1) induces pleural mesothelial cell (PMC) transformation into myofi

187 ) containing vesicle transportation in human pleural mesothelial cells (HPMCs).

188 Pleural mesothelial cells (PMCs), which are derived from

189 ough increased phosphorylation of Tyr-216 in pleural mesothelial cells and GSK-3beta mobilization fro

190 Pleural mesothelial cells contribute to pleural rind for

191 malignant mesothelial tissues and malignant pleural mesothelioma (MPM) cell lines as compared to ben

192 Malignant pleural mesothelioma (MPM) is a highly aggressive and ge

193 Malignant pleural mesothelioma (MPM) is a highly aggressive tumor

194 Malignant pleural mesothelioma (MPM) is an aggressive cancer that

195 Malignant pleural mesothelioma (MPM) is an aggressive cancer that

196 Malignant pleural mesothelioma (MPM) is an aggressive human cancer

197 Malignant pleural mesothelioma (MPM) is an aggressive neoplasm ass

198 Malignant pleural mesothelioma (MPM) is an aggressive thoracic can

199 Hemithoracic IMPRINT for malignant pleural mesothelioma (MPM) is safe and has an acceptable

200 ed in patients with ASS1-deficient malignant pleural mesothelioma (MPM) or non-small-cell lung cancer

201 targeted exomes (n = 103) from 216 malignant pleural mesothelioma (MPM) tumors.

202 therapy as first-line treatment of malignant pleural mesothelioma (MPM).

203 P) in the treatment of epithelioid malignant pleural mesothelioma (MPM).

204 rgoing cancer-directed surgery for malignant pleural mesothelioma (MPM); however, it is unclear if th

205 Patients with measurable advanced malignant pleural mesothelioma and disease progression after one o

206 ere on the interim analysis of the malignant pleural mesothelioma cohort.

207 results are in favor of an increased risk of pleural mesothelioma for subjects exposed to both asbest

208 Malignant pleural mesothelioma incidence continues to rise, with f

209 Malignant pleural mesothelioma is a highly aggressive cancer with

210 Malignant pleural mesothelioma is an aggressive malignancy charact

211 sed immunotherapy in patients with malignant pleural mesothelioma is feasible, well-tolerated, and ca

212 ria In Solid Tumors (RECIST) version 1.0 for pleural mesothelioma or RECIST version 1.1 for peritonea

213 Ten patients with malignant pleural mesothelioma received metronomic cyclophosphamid

214 ocedure-tract metastases (PTMs) in malignant pleural mesothelioma remains controversial, and clinical

215 port on their use of a murine model of human pleural mesothelioma to explore potential factors that l

216 benefit reported in patients with malignant pleural mesothelioma treated in a phase 1 study of vorin

217 eated patients with PD-L1-positive malignant pleural mesothelioma were enrolled from 13 centres in si

218 ients with pleural effusion due to malignant pleural mesothelioma, and talc pleurodesis might be pref

219 Using an orthotopic mouse model of pleural mesothelioma, we determined that relatively high

220 ed 68 with advanced ASS1-deficient malignant pleural mesothelioma.

221 therapy for patients with advanced malignant pleural mesothelioma.

222 talc pleurodesis in patients with malignant pleural mesothelioma.

223 os and silica seemed to increase the risk of pleural mesothelioma.

224 ty in patients with PD-L1-positive malignant pleural mesothelioma.

225 on in patients with ASS1-deficient malignant pleural mesothelioma.

226 Pleural mesothelium overlying the lymphatic plexuses und

227 cic cavity through exfoliated regions of the pleural mesothelium.

228 oneal seeding nodule from the primary tumor, pleural metastases, malignant pleural effusion, and asci

229 Here we show, using separate models of pleural nematode infection with Litomosoides sigmodontis

230 e pain and routine chest roentgenogram shows pleural nodular masses.

231 date patients in terms of pleural thickness, pleural nodules and loculation (p>0.05).

232 g pleural exudates from transudates included pleural nodules, pleural thickening and loculation.

233 The parietal pleural of TNF(-/-) and TNFR1R2(-/-) mice exhibited abun

234 s 19 countries in patients with unresectable pleural or peritoneal malignant mesothelioma who had pro

235 pleural lesions; 187 pulmonary lesions) had pleural origin or were peripherally located in the lung

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

237 sbestos is a well-known lung carcinogen, the pleural plaque-lung cancer link remains controversial.

238 mortality was significantly associated with pleural plaques in the follow-up study in terms of both

239 Pleural plaques may be an independent risk factor for lu

240 ancer mortality according to the presence of pleural plaques, with age as the main time variable, adj

241 SUVmax] range, 3.1-6.7) and 1 patient with a pleural plasmacytoma (SUVmax, 7.2); the remaining 3 pati

242 rect diagnosis was indicated on the basis of pleural pointillism in 88 patients (sensitivity, 93%; sp

243 Visual assessment of pleural pointillism on high-b-value DW images is useful

244 Pleural pointillism was denoted by the presence of multi

245 thorax volume decrease due to fibrosis), and pleural pointillism were examined.

246 al and laterolateral axes and the changes in pleural pressure (Ppl) and transdiaphragmatic pressure w

247 wall elastance-based methods for estimating pleural pressure and setting positive end-expiratory pre

248 wall elastance-based methods for estimating pleural pressure do not yield similar results.

249 The pleural pressure estimates using both methods were disco

250 isconceptions include assertions that normal pleural pressure must be negative (subatmospheric) and t

251 er ribs is equal to the expiratory effect of pleural pressure, and that the insertional force contrib

252 ease in change in airway pressure, change in pleural pressure, change in pericardial pressure, and ch

253 compare two published methods for estimating pleural pressure, one based on directly measured esophag

254 0.3 +/- 0.1 mm Hg/mL/kg for airway pressure, pleural pressure, pericardial pressure, and central veno

255 nges in Pes are representative of changes in pleural pressure.

256 oing mechanical ventilation due to increased pleural pressure.

257 , airway pressure, pericardial pressure, and pleural pressure; pulse pressure variations, systolic pr

258 surgical versus non-surgical procedure, and pleural procedure (indwelling pleural catheter vs other)

259 e safety of hemithoracic intensity-modulated pleural radiation therapy (IMPRINT) after chemotherapy a

260 Peritoneal and pleural resident macrophages in the mouse share common f

261 Pleural mesothelial cells contribute to pleural rind formation by undergoing mesothelial mesench

262 oracic notum as well as the expected medial, pleural series of axillary sclerites.

263 ract and subsequently degranulate MCs in the pleural space by elaborating CCL2 and osteopontin.

264 Pleural space infections are increasing in incidence and

265 ute by which pathogenic organisms access the pleural space is poorly understood.

266 (subatmospheric) and that a pressure in the pleural space may not be substantially positive when a s

267 lung infection, B1a B cells migrate from the pleural space to the lung parenchyma to secrete polyreac

268 eloid cells from the host bone marrow to the pleural space via the spleen.

269 The pleural space was insufflated with CO2 to displace the l

270 States every year, most often arising in the pleural space, but also occurring as primary peritoneal

271 Once homed to the pleural space, MCs released tryptase AB1 and IL-1beta, w

272 ncreased IFNgamma and TNFalpha levels in the pleural space.

273 ed by the presence of multiple, hyperintense pleural spots on high-b-value DW images.

274 argin and the other vg-dependent tissue, the pleural structures (trochantin and epimeron).

275 The ablation zone extended to the pleural surface adjacent to the heart in 71% of parallel

276 ifference between the alveolar space and the pleural surface), traditionally known as the "elastic re

277 the opening to the pulmonary airway and the pleural surface).

278 near pleural tag; type 2, one or more linear pleural tag with soft tissue component at the pleural en

279 nd type 3, one or more soft tissue cord-like pleural tag) and prioritized into types 3, 2, and 1 when

280 into three types (type 1, one or more linear pleural tag; type 2, one or more linear pleural tag with

281 Type 3 pleural tags indicated minimal increase in the likelihoo

282 Type 2 pleural tags on conventional CT images can increase the

283 Type 1 pleural tags provided weak evidence to rule out visceral

284 The presence of type 2 pleural tags was moderately associated with visceral ple

285 The pleural tags were classified into three types (type 1, o

286 In the absence of pleural tags, no pleural invasion was found.

287 ther findings included bronchiectasis (48%), pleural thickening (40%), ground glass opacity (32%), ma

288 gn vs malignant) on the basis of mediastinal pleural thickening (sensitivity, 81%; specificity, 73%;

289 ties were nodules, peribronchial thickening, pleural thickening and bronchiectasis.

290 s from transudates included pleural nodules, pleural thickening and loculation.

291 with Col-1 and alpha-smooth muscle actin in pleural thickening in the carbon-black bleomycin mouse m

292 Pleural thickening was also notably reduced in 9ING41-tr

293 brosis excess collagen deposition results in pleural thickening, increased stiffness and impaired lun

294 tion, the diagnostic accuracy of mediastinal pleural thickening, shrinking lung (hemithorax volume de

295 orming substantially better than mediastinal pleural thickness and shrinking lung, and might obviate

296 transudate and exudate patients in terms of pleural thickness, pleural nodules and loculation (p>0.0

297 lternative to the MGIT system for diagnosing pleural tuberculosis.

298 kiness and triggered NF-kappaB activation in pleural tumor cells, thereby fostering pleural fluid acc

299 tase AB1 and IL-1beta, which in turn induced pleural vasculature leakiness and triggered NF-kappaB ac

300 cond line vs third line), and anatomic site (pleural vs peritoneal), by use of an interactive voice o