ライフサイエンスコーパス: diaphragm

1 and reduced dystrophic histopathology in the diaphragm.

2 c protein, is the main component of the slit diaphragm.

3 ng initiating pore formation in a hemifusion diaphragm.

4 ntensity and inspiratory neural drive to the diaphragm.

5 nounced in the tibialis anterior than in the diaphragm.

6 creased expression of components of the slit diaphragm.

7 e for a loss of Pax7+ satellite cells in the diaphragm.

8 procedure that confirmed the rupture of the diaphragm.

9 ase channel/ryanodine receptor (RyR1) in the diaphragm.

10 ion and progressive fibrosis in the mdx(5cv) diaphragm.

11 dystrophin protein and exon skipping in the diaphragm.

12 uitin-proteasome pathway is activated in the diaphragm.

13 the podocyte intercellular junction, or slit diaphragm.

14 nd liver) suggest the presence of a muscular diaphragm.

15 iated virus vector delivered directly to the diaphragm.

16 sustained improvement of mdx(5cv)-Ccr2(-/-) diaphragm.

17 to invoke direct size selection by the slit diaphragm.

18 151 local recurrent HCC lesions abutting the diaphragm.

19 , but none are observed upstream of the slit diaphragm.

20 sustained in limb muscles than it is in the diaphragm.

21 eolytic activity and oxidative stress in the diaphragm.

22 ressive fibrosis and dysfunction of mdx(5cv) diaphragm.

23 r channels and effacement of nephrocyte slit diaphragms.

24 2 at mitochondrial membranes and at the slit diaphragm, a specialized cell junction at the filtration

25 f animals displaying recovery of ipsilateral diaphragm activity increased in AAV-TrkB-treated (9/9) c

26 ung-protective ventilation while maintaining diaphragm activity under partial ventilatory support.

27 rtial ventilatory support, while maintaining diaphragm activity, in sedated patients with lung injury

28 spite recognized benefits, such as preserved diaphragm activity, partial support ventilation modes ma

29 TS: Satellite cell depletion does not affect diaphragm adaptations to voluntary wheel running in youn

30 Co-localised images of diaphragm after TGF-alpha overexpression revealed a laye

31 Importantly, diaphragm amplitude again correlated strongly with ex vi

32 Also, diaphragm amplitude and specific force negatively correl

33 icro-dystrophin administration increased mdx diaphragm amplitude by 26% after 4 weeks.

34 We then investigated the time course of diaphragm amplitude changes following administration of

35 Diaphragm amplitude correlated positively with ex vivo f

36 In mdx mice, diaphragm amplitude decreased with age and values were m

37 Diaphragm amplitude peaked 4 weeks after AAV-muDys admin

38 Importantly, diaphragm amplitude strongly correlated with ex vivo spe

39 distinct hemifusion structures: a hemifusion diaphragm and a novel structure termed a 'lipidic juncti

40 we predominantly restored dystrophin in the diaphragm and assessed cardiac function by MRI.

41 ccompanied by segmental discontinuity of the diaphragm and collar sign.

42 or CT for penetrating torso trauma below the diaphragm and had surgically confirmed findings.

43 ransduction was seen in skeletal muscle, the diaphragm and heart for at least 4 months (the end of th

44 ship between peak electrical activity of the diaphragm and muscle pressure depicted a curvilinear pro

45 ect and systems-level evidence that the slit diaphragm and podocyte cytoskeleton are regulated target

46 Slit diaphragm and podocyte damage is crucial in the pathogen

47 dative stress and protein degradation in the diaphragm and prevents the reduction in contractility th

48 sion has been associated with descent of the diaphragm and protrusion of the anterior abdominal wall.

49 erved nephrin surface expression on the slit diaphragm and reduced proteinuria in diabetic mice, wher

50 In diaphragm and soleus muscles of the knockdown and knocko

51 Dystrophin insufficiency in the diaphragm and the longissimus resulted in muscle histopa

52 leave the esophagus to enter into the crural diaphragm and the remainder terminate into the sling fib

53 Atrophy was quantified in the diaphragm and tibialis anterior by measuring fiber diame

54 ons at neuromuscular junctions (NMJs) of the diaphragm and tibialis anterior muscle as prominent feat

55 teins nephrin and neph1 localize to the slit diaphragm and transduce signals in a Src family kinase F

56 chnique for recurrent small HCC abutting the diaphragm, and both CT-RFA and L-RFA are effective techn

57 ation, splay within the expanding hemifusion diaphragm, and fissure widening initiating pore formatio

58 al function, reduced oxidative stress in the diaphragm, and maintained normal diaphragm contractility

59 iaphragm atrophy, to strengthen an atrophied diaphragm, and mitigate the harms of mechanical ventilat

60 ey structural component of the podocyte slit diaphragm, and proper expression of nephrin on the cell

61 ation provided clear delineation of diseased diaphragm, and together with organ bath assessment, prov

62 apparatus in mice lacking the critical slit diaphragm-associated protein CD2AP, highlighting the gre

63 ment led to decreased expression of the slit diaphragm-associated proteins podocin, nephrin, and syna

64 ifications in the skeletal muscle, heart and diaphragm at 7 weeks, suggesting that their pathology is

65 essential for mechanical ventilation-induced diaphragm atrophy and contractile dysfunction.

66 oxO showed a significant attenuation of both diaphragm atrophy and contractile dysfunction.

67 Diaphragm atrophy and dysfunction have been reported in

68 n: the purpose of this study was to quantify diaphragm atrophy in a population of critically ill mech

69 ly the ventilation support was predictive of diaphragm atrophy rate.

70 ring catheter may provide a means to prevent diaphragm atrophy, to strengthen an atrophied diaphragm,

71 Fibers were isolated from diaphragm biopsies of 36 mechanically ventilated critica

72 ve primarily focused on early effects on the diaphragm by CMV, or at specific time points.

73 intercostal muscles (by 19% +/- 2%) and the diaphragm (by 18% +/- 4%), activated the internal obliqu

74 oduct podocin is a key component of the slit diaphragm cell junction at the kidney filtration barrier

75 ce of expansion of the diaphragm muscle, the diaphragm central tendon is reduced in size, likely cont

76 of inspiratory effort may prevent changes in diaphragm configuration associated with mechanical venti

77 Low diaphragm contractile activity was associated with rapid

78 ce were protected against the development of diaphragm contractile weakness during mechanical ventila

79 chanical ventilation independently decreased diaphragm contractility and fiber dimensions and increas

80 saline or lipopolysaccharide administration, diaphragm contractility was measured in vitro.

81 ress in the diaphragm, and maintained normal diaphragm contractility.

82 of abdominal distension were associated with diaphragm contraction (19% +/- 3% increase in EMG score

83 We report here that periodic diaphragm contraction via phrenic nerve stimulation (PNS

84 unction of the major inspiratory muscle, the diaphragm, contributing to ventilator dependence.

85 ting and renewal progeny than their limb and diaphragm counterparts.

86 al mammalian skeletal muscle, and defects in diaphragm development are the cause of congenital diaphr

87 nd muscle connective tissue are critical for diaphragm development, and mutations in PPF-derived fibr

88 among genes that are highly expressed during diaphragm development, there was a significant burden of

89 The rupture frequency and hemifusion diaphragm diameter were not affected by G1S mutation, bu

90 eading to aberrant nephrin turnover and slit diaphragm disassembly.

91 Prolonged satellite cell depletion in the diaphragm does not result in excessive extracellular mat

92 microm by 800 microm actuator has a silicon diaphragm driven by a piezoelectric thin film (e.g., lea

93 ould focus on the role of Pax3+ cells in the diaphragm during adaptation to exercise and ageing.

94 edation and, 2) metabolic changes within the diaphragm during mechanical ventilation compared to arti

95 en hypothesized that electrically pacing the diaphragm during mechanical ventilation could reduce dia

96 of transcription factors is activated in the diaphragm during mechanical ventilation, and forkhead bo

97 and regulate podocyte cytoskeleton and slit diaphragm dynamics, MAGI2 mutations have not been descri

98 Diaphragm dysfunction develops during severe sepsis as a

99 RATIONALE: Ventilator-induced diaphragm dysfunction is a significant contributor to we

100 Diaphragm dysfunction is twice as frequent as limb muscl

101 al ventilation (MV)-acquired limb muscle and diaphragm dysfunction may both be associated with longer

102 Diaphragm dysfunction was associated with higher ICU and

103 eathing trial after at least 24 hours of MV, diaphragm dysfunction was evaluated using twitch trachea

104 r first spontaneous breathing trial: 63% had diaphragm dysfunction, 34% had limb muscle weakness, and

105 tor, many of whom acquire ventilator-induced diaphragm dysfunction.

106 rapeutic target to combat ventilator-induced diaphragm dysfunction.

107 cal ventilation prevents ventilation-induced diaphragm dysfunction.

108 nerve pacing may mitigate ventilator-induced diaphragm dysfunction.

109 m during mechanical ventilation could reduce diaphragm dysfunction.

110 Diaphragm elastic modulus assessed by OCT-based indentat

111 Diaphragm elastic modulus at left and right lateral loca

112 2.5 to 10.7 +/- 1.2 cm H2O; P < 0.0001), and diaphragm electrical activity (17.4 +/- 2.3 to 4.5 +/- 0

113 Neural respiratory drive, measured as diaphragm electromyogram (EMGdi) activity expressed as a

114 Adult male Sprague-Dawley rats underwent diaphragm electromyography electrode implantation and SH

115 hing frequency (fb ) and rate of rise of the diaphragm EMG increased in 6 of 7 animals but the group

116 Hemifusion diaphragm expansion is spontaneous for distal monolayers

117 Intramuscular MPs in mdx(5cv)-Ccr2(-/-) diaphragm expressed a low level of IL-1beta, IL-6, and I

118 strategies that target the contractility of diaphragm fibers to facilitate weaning.

119 Diaphragm fibroblasts at 14 wk showed a similar cell num

120 ith ex vivo force values and negatively with diaphragm fibrosis, a major cause of DMD muscle weakness

121 kdown of dKank in nephrocytes disrupted slit diaphragm filtration structures and lacuna channel struc

122 g effacement and disorganization of the slit diaphragm, followed by foot process disappearance, flatt

123 functional and histological outcomes in the diaphragm following 12 months of treatment.

124 improve mitochondrial function in the human diaphragm following surgery/mechanical ventilation.

125 re muscle degeneration, simvastatin enhanced diaphragm force and halved fibrosis, a major cause of fu

126 Maximum diaphragm force in conventional organ bath studies was a

127 mdx diaphragm force is commonly assessed ex vivo, precluding

128 ndothelial protein with roles in endothelial diaphragm formation and maintenance of basal vascular pe

129 for podocyte foot process arborization, slit diaphragm formation, and proper nephrin trafficking.

130 Conversely, diaphragms formed from single-component distal monolayer

131 hydrolysis events induce axial excursions of diaphragm-forming central pore loops that effect the app

132 suprathreshold endplate potentials in mouse diaphragms fully intoxicated by BoNT/A.

133 g delivery system, which induces recovery of diaphragm function after SCI in the adult rat model.

134 restored life span, whole-body strength, and diaphragm function and increased muscle strength.

135 -alpha overexpression produces impairment in diaphragm function and, therefore, an increase in the wo

136 gmatic pathophysiology and markedly improved diaphragm function but did not improve cardiac function

137 Diaphragm function in mdx mice is commonly evaluated by

138 ique for measuring time-dependent changes of diaphragm function in mdx mice.

139 Therefore, accurate assessment of diaphragm function in vivo would provide an important ad

140 sessing time-dependent changes in dystrophic diaphragm function in vivo, and for evaluating potential

141 graphy to evaluate time-dependent changes in diaphragm function in vivo, by measuring diaphragm movem

142 for assessing time-dependent changes in mdx diaphragm function in vivo.

143 Resting in vivo diaphragm function was also unaffected by satellite cell

144 Maximal thickening fraction (a measure of diaphragm function) was lower in patients with decreased

145 eleton, ear, branchial arches, heart, lungs, diaphragm, gut, kidneys, and gonads.

146 to suggest that restoring dystrophin in the diaphragm improves both respiratory and cardiac function

147 tocol, transvenous stimulation activated the diaphragm in 22 of 23 (96%) left phrenic capture attempt

148 t of atrophy and contractile weakness of the diaphragm in critically ill patients.

149 recapitulates the evolutionary origin of the diaphragm in mammals.

150 enic nerve pacing therapy for protecting the diaphragm in sedated and ventilated pigs.

151 vely sensitive to electrical activity of the diaphragm in terms of triggering.

152 Thus, MV-induced diaphragm inactivity initiates catabolic changes via rap

153 Previous data from Stac3-deleted diaphragms indicated that Stac3-deleted skeletal muscle

154 d blood vascular network in the lung and the diaphragm, indicative of an angiogenetic defect.

155 Hoxa5 in motor neurons resulted in abnormal diaphragm innervation and musculature, and lung hypoplas

156 s podocyte shape, structure, stability, slit diaphragm insertion, adhesion, plasticity, and dynamic r

157 2 leads to excessively long myofibers in the diaphragm, intercostal and levator auris muscles but not

158 soft palate, pharynx, and larynx as well as diaphragm, intercostal, abdominal, and pelvic floor musc

159 ractility and fiber dimensions and increased diaphragm interleukin-6 production, protein ubiquitinati

160 oglossus), jaw (digastric), and respiration (diaphragm, internal intercostal, external abdominal obli

161 The diaphragm is an essential mammalian skeletal muscle, and

162 The diaphragm is an important regulator of expiration.

163 In conclusion, whilst the diaphragm is an important respiratory muscle, it is like

164 The diaphragm is derived from multiple embryonic sources, bu

165 ircumferential squeeze of the LES and crural diaphragm is generated by a unique myo-architectural des

166 T: Satellite cell contribution to unstressed diaphragm is higher compared to hind limb muscles, which

167 ratory and cardiac function, the role of the diaphragm is not well understood.

168 null mutants, indicating that the defective diaphragm is the main cause of impaired survival at birt

169 RATIONALE: The diaphragm is the major inspiratory muscle and is assumed

170 onic sources, but how these give rise to the diaphragm is unknown, and, despite the identification of

171 ervating the limbs, intercostal muscles, and diaphragm, is predominantly responsible for this fatal p

172 flammatory response, but its role within the diaphragm itself during sepsis is unknown.

173 Diaphragm lactate release increased in CMV transiently w

174 t recloses afterward, suggesting a molecular diaphragm-like mechanism to control DNA efflux.

175 he Pals1 ortholog caused alterations in slit-diaphragm-like structures.

176 magnitude higher than those of conventional diaphragm materials (e.g., silica, silver films).

177 Satellite cell depletion did not alter diaphragm mean fibre cross-sectional area, fibre type di

178 ecialized cell junction at the podocyte slit diaphragm, MEC-2 is found in neurons required for touch

179 the striking migration of PPF cells controls diaphragm morphogenesis.

180 Coq2, the silencing of which disrupted slit diaphragm morphology.

181 am tsDCS delivered to the C3-C5 level on (1) diaphragm motor-evoked potentials (DiMEPs) elicited by t

182 Diaphragm movement amplitude values for mdx mice were co

183 in diaphragm function in vivo, by measuring diaphragm movement amplitude.

184 Diaphragm MPs from both mdx(5cv)-Ccr2(-/-) and mdx(5cv)

185 both young and aged satellite cell-depleted diaphragm muscle (P < 0.05), which may compensate for th

186 Spontaneous recovery of ipsilateral diaphragm muscle activity is associated with increased p

187 we hypothesize that recovery of ipsilateral diaphragm muscle activity post-SH, whether spontaneous o

188 mproved muscle pathology and function in mdx diaphragm muscle at early stages.

189 We obtained diaphragm muscle biopsies from 22 critically ill patient

190 The mdx diaphragm muscle closely mimics the pathophysiological c

191 CCR2 deficiency reduced quadriceps and diaphragm muscle damage and fibrosis at 14 wk but not at

192 ng the major effectors of ventilator-induced diaphragm muscle dysfunction (VIDD), but the upstream in

193 Critically ill patients have manifest diaphragm muscle fiber atrophy and weakness in the absen

194 on results in a significant decrease in both diaphragm muscle fiber size and diaphragm-specific force

195 Diaphragm muscle fibers from critically ill patients dis

196 We hypothesized that weakness of diaphragm muscle fibers in critically ill patients is ac

197 These findings show that diaphragm muscle fibers of critically ill patients displ

198 Both slow- and fast-twitch diaphragm muscle fibers of critically ill patients had a

199 We hypothesized that diaphragm muscle fibers of mechanically ventilated criti

200 ial function, and mitochondrial structure in diaphragm muscle fibers.

201 This enhanced the diaphragm muscle force, to a greater extent with lower l

202 ased transsynaptic tracing strategy from the diaphragm muscle in the mouse, that the principal inspir

203 The mdx diaphragm muscle most closely recapitulates key features

204 Upon injection into the diaphragm muscle of rats, we show that the nanoconjugate

205 is at 14 wk but not at 6 mo, and it improved diaphragm muscle regeneration and respiratory function a

206 tibialis anterior (TA) muscles (in situ) or diaphragm muscle strips (in vitro).

207 aphragmatic dysfunction (VIDD) refers to the diaphragm muscle weakness that occurs following prolonge

208 ts, but as a consequence of expansion of the diaphragm muscle, the diaphragm central tendon is reduce

209 es reductions in TrkB kinase activity in the diaphragm muscle.

210 le fibers, and improved strength of the weak diaphragm muscle.

211 ctional roles in the advancement of MD using diaphragm muscles from mdm (MD with myositis) mice, an a

212 antly alters the miRNA expression profile in diaphragm muscles from WT and mdm mice; as a result, som

213 T) and Ccr2(-/-) mice, and in quadriceps and diaphragm muscles of mdx(5cv) mice, a mouse model for Du

214 Diaphragm muscles were analysed from young (8 months) an

215 jured muscles and in mdx(5cv) quadriceps and diaphragm muscles.

216 e loss of function of slow-twitch soleus and diaphragm muscles.

217 tion of the respiratory rhythm generator and diaphragm neuromuscular junctions appeared normal.

218 in central nervous system synapses and mouse diaphragm neuromuscular junctions fully intoxicated by B

219 and severe contractile weakness, and in the diaphragm of critically ill patients the ubiquitin-prote

220 thway were significantly up-regulated in the diaphragm of critically ill patients.

221 in situ hybridization we show here that the diaphragm of FgfrL1 knockout animals lacks any slow musc

222 ted the potential protective effect upon the diaphragm of inhibiting nuclear factor-kappaB only withi

223 m following intramuscular injection into the diaphragm of rats.

224 ysis, autophagy, and oxidative stress in the diaphragm of septic rats.

225 stress at the circumference of the hemifused diaphragm of the prepore intermediate state.

226 hanged in TA muscles of treated mdx mice and diaphragm of treated mdx and dko mice.

227 on at the most highly fragmented NMJs in the diaphragms of old (26-28 months) mice is, if anything, s

228 eviously shown to result in loss of the slit diaphragms of the podocytes, leading to the hypothesis t

229 s of let-7e-5p in myocytes isolated from the diaphragms of WT and mdm mice confirmed Col1a1, Col1a2,

230 e the high glycogen content of the heart and diaphragm or impaired wirehang performance.

231 rosis persisted at 20 mo in leg (p = 0.038), diaphragm (p = 0.042), and heart muscles (p < 0.001).

232 In this First-in-Human series, diaphragm pacing with a temporary catheter was safe and

233 A-HRP, AuNPs, and drugs for the treatment of diaphragm paralysis associated with high cervical spinal

234 Unilateral diaphragm paralysis was identified in 3 infants.

235 life (4 months of age) has minimal effect on diaphragm phenotype by old age (24 months).

236 In this paper, a microfluidic tactile diaphragm pressure sensor based on embedded Galinstan mi

237 DMS) wristband with an embedded microfluidic diaphragm pressure sensor capable of real-time pulse mon

238 For larger diaphragms, prior studies have shown that pore expansion

239 is a key protein of the kidney podocyte slit diaphragm protein complex, an important part of the glom

240 The prohibitin homology domain of the slit diaphragm protein podocin contained one such site, threo

241 Expression of several key slit diaphragm protein was down regulated in pGR KO mice.

242 tein, essential for the assembly of the slit diaphragm protein-lipid supercomplex.

243 ntracellular movements of this critical slit diaphragm protein.

244 n CDH, expression profiles of the developing diaphragm, protein interaction networks expanded from th

245 a(2+) influx, oxidative stress, loss of slit diaphragm proteins, and apoptosis.

246 Here, we discovered that two Drosophila slit diaphragm proteins, orthologs of the human genes encodin

247 ction in dystrophin protein abundance in the diaphragm, psoas major, and longissimus lumborum and a 5

248 3.5 L/min, compressed using a small on-board diaphragm pump.

249 the lens chamber using servo motor actuated diaphragm pumps.

250 satellite cell depletion negatively impacts diaphragm quantitative and qualitative characteristics u

251 We identify a diaphragm radius, below which central pore expansion is

252 embryonic structures, are the source of the diaphragm's muscle connective tissue and regulate muscle

253 there is no definitive evidence to show slit diaphragm (SD) to TJ transition in vivo Here, we report

254 a block containing the human LES and crural diaphragm, serially sectioned at 50 mum intervals and im

255 ly induced neuromechanical uncoupling of the diaphragm should facilitate lung-protective ventilation

256 ed sometimes when electrical activity of the diaphragm signal depicted a biphasic aspect, and an abno

257 on, attenuates muscle pathology and improves diaphragm, skeletal muscle and cardiac function.

258 positive lineage origin) with their limb and diaphragm somite-derived counterparts, but are remarkabl

259 ease in both diaphragm muscle fiber size and diaphragm-specific force production.

260 ipid components, given sufficiently negative diaphragm spontaneous curvature.

261 In cocultures, fibrocytes from the mdx(5cv) diaphragm stimulated a higher level of fibroblast expres

262 sent study demonstrates novel changes in the diaphragm structure/function and underlying mechanisms a

263 There was a nonsignificant decrease in diaphragm tetanic force production over the experiment i

264 tokines was significantly higher in mdx(5cv) diaphragm than in mdx(5cv) quadriceps.

265 sis triggered transient fiber atrophy in the diaphragm that lasted for 24 hours and prolonged atrophy

266 microscopy, we present images of hemifusion diaphragms that form as stalks expand and propose a mode

267 ower in patients with decreased or increased diaphragm thickness (n = 10) compared with patients with

268 le activity was associated with increases in diaphragm thickness (P = 0.002).

269 Diaphragm thickness and contractile activity (quantified

270 Changes in diaphragm thickness are common during mechanical ventila

271 Diaphragm thickness assessed by ultrasound and normalize

272 Over the first week of ventilation, diaphragm thickness decreased by more than 10% in 47 (44

273 causes, and functional impact of changes in diaphragm thickness during routine mechanical ventilatio

274 mouse diaphragm was measured from changes in diaphragm thickness in response to an applied force prov

275 Diaphragm thickness in the zone of apposition was measur

276 Pressure support predicted diaphragm thickness with coefficient -0.006 (95% CI, -0.

277 ivity was associated with rapid decreases in diaphragm thickness, whereas high contractile activity w

278 g the activation of forkhead boxO in the rat diaphragm through the use of a dominant-negative forkhea

279 Together, our results validate diaphragm ultrasonography as a reliable technique for as

280 These studies validate diaphragm ultrasonography as a reliable technique for as

281 onstrate that loss of NDST1 causes defective diaphragm vascular development and CDH and that heparan

282 ed indentation, the elastic modulus of mouse diaphragm was measured from changes in diaphragm thickne

283 To date, the nature of diaphragm weakness and its underlying pathophysiologic m

284 The mechanisms underlying diaphragm weakness are unknown, but might include mitoch

285 The clinical significance of diaphragm weakness in critically ill patients is evident

286 RATIONALE: The clinical significance of diaphragm weakness in critically ill patients is evident

287 sponsible for mechanical ventilation-induced diaphragm weakness is essential to developing effective

288 evelopment of mechanical ventilation-induced diaphragm weakness remains unknown.

289 prolonged mechanical ventilation results in diaphragm weakness, which contributes to problems in wea

290 stability in the control of breathing due to diaphragm weakness.

291 essures, and peak electrical activity of the diaphragm were continuously recorded.

292 ever, the opposite effect is observed in the diaphragm, where NCX1 overexpression mildly protects fro

293 The muscle fascicles of the right crus of diaphragm which form the esophageal hiatus are arranged

294 erminant of the structural integrity of slit diaphragm, which is a critical component of kidney's fil

295 is a unique cell junction known as the slit diaphragm, which is physically connected to the actin cy

296 entilation alters the metabolic state of the diaphragm, which might be one pathophysiologic origin of

297 aphy include: segmental discontinuity of the diaphragm with herniation through the rupture, dependent

298 We therefore challenged the diaphragm with prolonged running activity in the presenc

299 liver, pancreas, skeletal muscle, heart and diaphragm without causing significant histopathological

300 ery there was only partial relaxation of the diaphragm, without rupture.