ライフサイエンスコーパス: septal

1 c cardiomyopathy patients undergoing alcohol septal ablation (ASA) and surgical septal myectomy (SM)

2 enty years after the introduction of alcohol septal ablation (ASA) for the treatment of obstructive h

3 ce of arrhythmic complications after alcohol septal ablation (ASA) is unclear.

4 However, the results of alcohol septal ablation are dependent on the septal perforator a

5 Alcohol septal ablation is a less invasive treatment.

6 on of the prosthesis, and successful alcohol septal ablation was performed.

7 eptal reduction therapy (myectomy or alcohol septal ablation) is recommended.

8 43 days) after surgical myectomy (or alcohol septal ablation), 92% and 95% of patients with or withou

9 choice between surgical myectomy and alcohol septal ablation.

10 , either surgical septal myectomy or alcohol septal ablation.

11 Septal activation in patients with left bundle-branch bl

12 proteins to samples from patients undergoing septal alcohol ablation for hypertrophic cardiomyopathy,

13 the septum; in turn, EBGNs were targeted by septal and entorhinal inputs.

14 ort the dynamics of FtsZ movement leading to septal and equatorial ring formation in the ovoid-shaped

15 ence limits for TDI e' (4.6 and 5.2 cm/s for septal and lateral TDI e', respectively) were substantia

16 es in all four LV ROIs (anterior, posterior, septal and lateral wall, 99 +/- 2, 94 +/- 5, 94 +/- 4 an

17 In oval-shaped Streptococcus pneumoniae, septal and longitudinal peptidoglycan syntheses are perf

18 Regarding location and pattern, septal and midwall LGE showed strongest associations wit

19 ovoid-shaped Streptococcus pneumoniae (Spn), septal and peripheral (elongation) PG synthesis occur si

20 proposed as molecular switches that balance septal and peripheral (side-wall like) peptidoglycan (PG

21 attributed to PFO with an associated atrial septal aneurysm or large interatrial shunt, the rate of

22 attributed to PFO, with an associated atrial septal aneurysm or large interatrial shunt, to transcath

23 ge; study period; device; presence of atrial septal aneurysm, hypertension, hyperlipidemia, diabetes,

24 la (30), accessory auricular appendages (5), septal aneurysms (8), septal bags (6) and 1 thrombus in

25 d as follows: -179 + log(e) interventricular septal angle x 42.7 + log(10) ventricular mass index (ri

26 lar stroke volume, isovolumic relaxation, E' septal annulus, E/E' septal annulus, left ventricular di

27 ovolumic relaxation, E' septal annulus, E/E' septal annulus, left ventricular diastolic volume).

28 via projections from the hippocampus to the septal area.

29 re also borderline amygdalar, claustral, and septal areas of the pallium, nuclear in structure.

30 osensory cortical map, affecting barrel, and septal areas.

31 icular appendages (5), septal aneurysms (8), septal bags (6) and 1 thrombus in the left atrial append

32 entify the types of tissues found in a nasal septal biopsy, i.e., hyaline cartilage and perichondrium

33 he membrane that treadmill to distribute the septal biosynthetic machinery.

34 %), papillary muscle (n=3; 3.1%), and apical-septal bundle (n=1; 1.0%), as well as imaging plane obli

35 terior to the right globe, predominantly pre-septal but with slight post-septal extension.

36 s bundle pacing (HBP), and right ventricular septal capture in routine clinical practice.

37 between S-HBP, NS-HBP, and right ventricular septal capture morphologies by careful analysis of devic

38 that appears to be universally essential for septal cell wall assembly(5,6).

39 directing the spatiotemporal distribution of septal cell wall remodeling enzymes through the Z-ring's

40 powered by GTP hydrolysis and guides correct septal cell wall synthesis and cell division.

41 namics direct the processive movement of the septal cell wall synthesis machinery but do not limit th

42 g provides a mechanism for achieving uniform septal cell wall synthesis to enable correct polar morph

43 dinating an ensemble of proteins involved in septal cell wall synthesis to ensure successful constric

44 e of the Z-ring and its role in coordinating septal cell wall synthesis, the early stages of protofil

45 d recruits downstream proteins essential for septal cell wall synthesis.

46 ecular composition and ultrastructure of the septal cell wall were substantially altered.

47 The septal cells stained for vesicular acetylcholine transpo

48 Both the number of septal cells with cholinergic phenotype and their densit

49 epletion of GpsB prevents PBP2x migration to septal centers.

50 states that differ with respect to theta and septal cholinergic activity, and modulated at sharp wave

51 he total number, density, and soma volume of septal cholinergic cells, which were visualized in brain

52 sense the wakefulness-dependent activity of septal cholinergic fibers through the alpha7-nicotinic a

53 while modulating the excitability of medial septal cholinergic neurones.

54 Chemogenetic activation of septal cholinergic neurons expressing the excitatory hM3

55 Modifying septal cholinergic tone in this way also led mice to exh

56 uration, His-ventricular (HV) intervals, and septal conduction patterns were analyzed.

57 A total of 88 left septal conduction recordings were analyzed in 85 patient

58 formed detailed intracardiac mapping of left septal conduction to assess for the presence and level o

59 Heterogeneous septal conduction was observed in patients with surface

60 ith ATTR (70% sigmoid septum and 30% reverse septal contour), whereas symmetrical LVH was present in

61 ve patients were more likely to have reverse septal curvature morphology, LGE, and no significant res

62 utation positive and more likely had reverse septal curvature morphology, more fibrosis, but less res

63 The presence of a ventricular septal defect ( P=0.009) and older age at surgery ( P=0.

64 aOR = 1.28; 95% CI: 1.03, 1.61), ventricular septal defect (aOR = 1.19; 95% CI: 1.00, 1.43), and tetr

65 sitively associated with the risks of atrial septal defect (aORs ranging from 1.29 to 2.17), patent d

66 Familial atrial septal defect (ASD) has previously been attributed prima

67 Secundum atrial septal defect (ASD) is the most common adult congenital

68 offspring with a perimembranous ventricular septal defect (odds ratio = 3.23, 95% confidence interva

69 eft superior vena cava (P=0.85), ventricular septal defect (P=0.12), and bicuspid aortic valve (P=0.1

70 The superior sinus venosus atrial septal defect (SVASD) is characterized by deficiency of

71 Transcatheter ventricular septal defect (VSD) closure is a safe and efficacious al

72 Ventricular septal defect (VSD) is a lethal complication of acute my

73 erved an increased risk of CHDs, ventricular septal defect (VSD), and tetralogy of fallot (TF) with i

74 severe, excluding cases with isolated atrial septal defect and/or patent foramen ovale.

75 Between 2008 and 2012, atrial septal defect closure with the AMPLATZER Septal Occluder

76 r mille to 4.1 per mille, and of ventricular septal defect from 3.6 per mille to 4.5 per mille.

77 ffected offspring shared an atrioventricular septal defect or a common atrium along with postaxial po

78 ventricular septum and TGA with ventricular septal defect performed from 2010 to 2013.

79 ents immediately prior to an elective atrial septal defect repair procedure.

80 evalence of the diagnosis of secundum atrial septal defect rose from 2.3 per mille in 2000-2001 to 7.

81 Closure of atrial septal defect with the AMPLATZER Septal Occluder is safe

82 ricuspid regurgitation, residual ventricular septal defect) reduces this protective association.

83 ersistent truncus arteriosus and ventricular septal defect), hypoplastic lungs, hypoplastic/ectopic k

84 a and microcephaly), heart (atrioventricular septal defect), skeleton (postaxial polydactyly, narrow

85 tidiastole of coronary heart disease, atrial septal defect, and atrial fibrillation are made, and the

86 ncluding Ebstein's anomaly, atrioventricular septal defect, and others.

87 ients (6%) in the pitavastatin group (atrial septal defect, chronic obstructive pulmonary disease, ch

88 to be diagnosed via imaging (secundum atrial septal defect, patent ductus arteriosus, ventricular sep

89 efect, patent ductus arteriosus, ventricular septal defect, pulmonary artery anomalies, pulmonary val

90 eptum and 298 (38%) for TGA with ventricular septal defect.

91 pproaches for simple lesions, such as atrial septal defect.

92 tricular septal defects (22/47, 47%), atrial septal defects (20/47, 43%), patent ductus arteriosus (1

93 rdiovascular anomalies, of which ventricular septal defects (22/47, 47%), atrial septal defects (20/4

94 s (aRR, 0.85; 95% CI, 0.75-0.96), and atrial septal defects (aRR, 0.82; 95% CI, 0.69-0.95) but not se

95 (aRR, 0.77; 95% CI, 0.61-0.96), ventricular septal defects (aRR, 0.85; 95% CI, 0.75-0.96), and atria

96 1 and STX18, has been associated with atrial septal defects (ASD) in multiple European and Chinese co

97 ysiology and 12 control patients with atrial septal defects (ASD) that underwent cardiac catheterizat

98 Atrioventricular septal defects (AVSD) are a severe congenital heart defe

99 mon diagnoses were Ebstein's anomaly (n=44), septal defects (n=39), and single ventricle (n=36).

100 Ventricular septal defects (VSDs) were associated with the highest b

101 fects within it, termed muscular ventricular septal defects (VSDs), are common, yet less is known abo

102 transposition of the great arteries, atrial septal defects [ASD], aortic arch defects, and single-ve

103 nt in magnitude were detected between atrial septal defects and bromoform (aOR = 1.56; 95% CI: 1.01,

104 xclusively to Lipid II binding, which causes septal defects and catastrophic cell envelope damage.

105 X5, another transcription factor that causes septal defects when mutated.

106 erior cervical vertebral synostosis, cardiac septal defects with valve dysplasia, and deafness with i

107 % CI, -0.74 to -0.09); and major ventricular septal defects, -0.25 (95% CI, -0.35 to -0.15).

108 interval, -0.87 to -0.10); major ventricular septal defects, -0.41 (95% confidence interval, -0.52 to

109 9 kindreds with familial CHD, 4 with atrial septal defects, 2 with patent ductus arteriosus, 2 with

110 yndrome of progressive RCM, atrioventricular septal defects, and a high prevalence of atrial fibrilla

111 rt chambers, interatrial or interventricular septal defects, pericardium, and site and size of the gr

112 uding abnormalities of other cardiac valves, septal defects, persistent left superior vena cava, and

113 ased between 1990 and 2011 except for atrial septal defects, which increased significantly.

114 for percutaneous closure of secundum atrial septal defects.

115 ts paralog Hoxa1 results in atrioventricular septal defects.

116 lateral maxillary sinusitis in patients with septal deviation (p=0.007).

117 Neither septal deviation (right sided: p=0.962; left-sided: p=0.

118 oncha bullosa and contralateral direction of septal deviation [right-sided (p=0.039), left-sided (p=0

119 study was to assess if the presence of nasal septal deviation and concha bullosa is connected with th

120 Nasal septal deviation was found in 79.9% of computed tomograp

121 Nasal septal deviation, contrary to concha bullosa, has influe

122 presence of concha bullosa and direction of septal deviation.

123 % [14%], P < .001), whereas interventricular septal diameter was higher (mean [SD], 16 [3] vs 14 [2]

124 entricular tachycardia, unexplained syncope, septal diameter z-score, left ventricular posterior wall

125 tricular ejection fraction, interventricular septal diameter, mean limb lead QRS voltage, and grade 3

126 verity of disease, causing cardiac valve and septal disease in the neonate that was similar to the ra

127 ed for StkP localization or FDAA labeling at septal division rings.

128 c dimension z score of -1.85 or higher and a septal E' velocity z score less than -0.52 as having 74%

129 ecreased LV systolic, diastolic diameter, or septal E' velocity; higher ratio of LVWT to diastolic di

130 re cardiac mechanics: diastolic (lateral and septal E/e') and systolic (global longitudinal, radial,

131 ssembly and reabsorption of pericellular and septal elastic fibres, and a potential role for stratifi

132 elastosis contained oxytalan fibres, whereas septal elastosis at more advanced stages contained mainl

133 Early septal elastosis contained oxytalan fibres, whereas sept

134 Septal elastosis increased from intermediate to advanced

135 Septal elastosis is a gradual process with a transition

136 is (PCE)] and within bridging fibrous septa (septal elastosis) and scored using a semiquantitative sy

137 erformed RNA sequencing on right ventricular septal endomyocardial biopsies prospectively obtained fr

138 t, Panx1 knockout, and wild-type mouse nasal septal epithelial cells were grown at an air-liquid inte

139 roteins, exposed galactose on the surface of septal epithelial cells, thereby increasing its availabi

140 redominantly pre-septal but with slight post-septal extension.

141 py confirmed unusual mineral deposits in the septal extracellular matrix of the mutant mice.

142 Background Ventricular septal flattening, frequently present in pulmonary hyper

143 ditionally does not account for postsystolic septal flattening, often seen in PH.

144 re of maximal EI to account for postsystolic septal flattening, to establish the relationship with co

145 We report a specialized population of septal GABAergic neurons, the Teevra cells, selectively

146 ver from uniform lateral growth to localized septal growth is observed.

147 nal study of 69 patients (18 amyloidosis, 30 septal HCM, 6 apical HCM, and 15 controls) who underwent

148 eft ventricular wall thickness (amyloidosis, septal HCM, and apical HCM).

149 ional strain variation: cardiac amyloidosis, septal HCM, and apical HCM.

150 RI) was defined by lateral length divided by septal height.

151 previously unidentified LEC > hippocampus > septal higher-order circuit that regulates feeding behav

152 unusual elongation of the distal CA1 of the septal hippocampus.

153 wall thickness such as cardiac amyloidosis, septal hypertrophic cardiomyopathy (HCM), and apical HCM

154 Severe septal hypertrophy before ASA remained a marker of reduc

155 atients undergoing transcoronary ablation of septal hypertrophy removed spurious correlations between

156 negative and more likely had isolated basal septal hypertrophy with obstruction, but less fibrosis.

157 tive were more likely to have isolated basal septal hypertrophy, less LGE, and more LVOT obstruction.

158 After transcoronary ablation of septal hypertrophy, muscle-enriched miRNAs (miR-1 and mi

159 spike sequences in the form of a SPW-R when septal inhibition is removed; (3) generate and refine hi

160 Medial septal inputs to the hippocampal system are crucial for

161 ation between calcein transfer, SepJ-related septal junctions, and septal peptidoglycan nanopores.

162 oglycan perforations that likely accommodate septal junctions.

163 eak longitudinal strain was obtained for the septal, lateral, anterior, and inferior myocardial walls

164 of anterior-posterior (-0.31 +/- 0.4 cm) and septal-lateral dimensions (-0.21 +/- 0.3 cm), a decrease

165 Unlike cardiac AL amyloidosis, asymmetrical septal left ventricular hypertrophy (LVH) was present in

166 igns favoring PLC on HRCT (smooth or nodular septal lines, subpleural nodularity, peribronchovascular

167 icted in the correct chamber more often than septal locations (97% versus 79%, P=0.01).

168 of SPW-Rs on the firing patterns of lateral septal (LS) neurons in behaving rats.

169 e interventricular septum, referred to as LV septal (LVs) pacing, was demonstrated.

170 Left septal mapping was performed with a linear multielectrod

171 y which SpoIIQ specifically localizes to the septal membranes on the forespore side has remained enig

172 ounders, each unit decrease in peak systolic septal mitral annular velocity (Septal S') indicating po

173 val, 1.57-5.00; P=0.0005), and nonasymmetric septal morphology (odds ratio, 3.41; 95% confidence inte

174 olume, pulmonic outflow and interventricular septal motion may provide valuable insights into IUGR ca

175 Rhythmic medial septal (MS) GABAergic input coordinates cortical theta o

176 3 (LC3)-II protein levels were higher in HCM septal myectomies than in nonfailing control hearts and

177 g alcohol septal ablation (ASA) and surgical septal myectomy (SM) with patient management in accordan

178 undle branch block is a common sequela after septal myectomy but does not influence post-operative mo

179 hic cardiomyopathy who underwent transaortic septal myectomy from 1961 to 2016 were analyzed.

180 he perioperative mortality rate for isolated septal myectomy in most centers is <1%.

181 anch block are recognized sequelae following septal myectomy in patients with hypertrophic cardiomyop

182 ed operators working in high-volume centers, septal myectomy is highly effective with a >90% relief o

183 th septal reduction therapy, either surgical septal myectomy or alcohol septal ablation.

184 ively characterize sarcomeric proteoforms in septal myectomy tissues from HCM patients exhibiting sev

185 in the myocardium of HCM patients undergoing septal myectomy were remarkably consistent, regardless o

186 9 patients, all of whom had MV surgery (with septal myectomy).

187 d clinical results are comparable to that of septal myectomy.

188 s with a clinical diagnosis of HCM underwent septal myectomy.

189 medication for symptoms; 2 (4%) underwent a septal myectomy; 14 (25%) received an implantable cardio

190 in the apex and also in the subpopulation of septal myocytes that lack fast transient outward current

191 l fast-twitch and slow fibers via medial and septal nerves, followed by "s-type" units, which exclusi

192 innervate superficial slow muscle fibers via septal nerves.

193 firing parvalbumin-positive GABAergic medial septal neurons are strongly coupled to theta oscillation

194 ion of cortical cells and regions by diverse septal neurons are unknown.

195 However, a large population of medial septal neurons of unidentified neurotransmitter phenotyp

196 theta generation through local modulation of septal neurons.

197 ectrophysiological patch-clamp recordings of septal neurons.

198 The septal nuclei and forebrain were shown as the initial ke

199 more in the medial prefrontal cortex and the septal nuclei, both of which are targets of BF PV+ neuro

200 ical regions, hippocampus, amygdala, lateral septal nuclei, certain hypothalamic and midbrain nuclei,

201 imbic structures such as the amygdala or the septal nuclei.

202 cy of each distinct cell type in the lateral septal nucleus (LSN) region of mouse forebrain.

203 in the olfactory tubercle, striatum, medial septal nucleus, vertical and horizontal limbs of the dia

204 larger balloon-sized ASD diameter, Amplatzer septal occluder device size, and device size-ASD diamete

205 ata on patients implanted with the AMPLATZER Septal Occluder for percutaneous closure of secundum atr

206 rm safety and effectiveness of the AMPLATZER Septal Occluder in clinical practice are not available.

207 e of atrial septal defect with the AMPLATZER Septal Occluder is safe and effective.

208 ial septal defect closure with the AMPLATZER Septal Occluder was attempted in 1000 patients (aged 0.3

209 de that only right ventricle (RV) myocardial septal pacing is present.

210 between S-HBP, NS-HBP, and right ventricular septal pacing with a cumulative positive predictive valu

211 variate Cox regression analysis, the midwall septal pattern of LGE and the presence of LGE without ed

212 particularly when distributed with a midwall septal pattern.

213 In addition, we delineated the motion of the septal PBP2x transpeptidase and its FtsW glycosyl transf

214 orks with its cognate class B PBP to produce septal peptidoglycan during cell division.

215 Importantly, these phenotypes depend on septal peptidoglycan hydrolysis.

216 We show that the septal peptidoglycan is not completely degraded at the o

217 transfer, SepJ-related septal junctions, and septal peptidoglycan nanopores.

218 tained an increased number of nanopores, the septal peptidoglycan perforations that likely accommodat

219 cell-specific transcription, which initiates septal peptidoglycan remodeling involving synthetic and

220 ination between chromosome translocation and septal peptidoglycan remodeling to maintain spore develo

221 Loss of Ami1 resulted in defects in septal peptidoglycan turnover with release of excess cel

222 aments of FtsZ and FtsA (FtsAZ) that recruit septal peptidoglycan-synthesizing enzymes to the divisio

223 Interventricular septal perforation occurred (as late sequela) after 2 we

224 alcohol septal ablation are dependent on the septal perforator artery supplying the area of the conta

225 e is that ASA is limited by the route of the septal perforators, whereas myectomy is not.

226 r ring) and the leading-edge (inner ring) of septal PG (sPG) synthesis.

227 In Escherichia coli, septal PG synthesis and cell constriction rely on the ac

228 by FtsN, which may contribute to the overall septal PG synthesis and regulation during cell division.

229 The divisome controls septal PG synthesis and separation of daughter cells.

230 is tightly coupled to and limiting for both septal PG synthesis and septum closure in some bacteria,

231 the downstream division proteins but blocks septal PG synthesis until a signal is received that divi

232 ics and associations organize and distribute septal PG synthesis, but do not control its rate in S. p

233 sA to promote divisome assembly and regulate septal PG synthesis.

234 has implications for the local structure of septal PG, suggesting that there may be glycan bridges b

235 RodA-PBP3 and FtsW-PBP1 mediate sidewall and septal PGN incorporation, respectively, and that their a

236 ereas depletion of FtsW-PBP1 arrested normal septal PGN incorporation.

237 It forms a septal pore disc structure, recruits Spa18 and ApsB to s

238 n which SpoIIIE is anchored at the edge of a septal pore, stabilized by newly synthesized peptidoglyc

239 Compared with an apical position, an RV septal position of the LP was associated with increased

240 l organism Anabaena sp. strain PCC 7120, the septal protein SepJ is required for filament integrity,

241 ersing tissue planes (atrial and ventricular septal puncture, radiofrequency valve repair, transcaval

242 ive analysis of patients undergoing surgical septal reduction strategies was conducted in 3 European

243 symptoms related to ventricular obstruction, septal reduction therapy (myectomy or alcohol septal abl

244 Use of septal reduction therapy and the effect of institutional

245 Both techniques of septal reduction therapy are highly operator dependent.

246 These patients can be treated with septal reduction therapy, either surgical septal myectom

247 e, Siglec-1 expression was identified in the septal region of several affected fetal hearts.

248 prefrontal cortices, amygdala, hippocampus, septal region, and hypothalamus).

249 Septal regions of interests were used to determine T2 an

250 rgic neurons neurons project to two distinct septal regions: the dorsal and intermediate region of th

251 Surgery in which the heart was opened (e.g., septal repair) versus surgery in which it was not (e.g.,

252 ce area of the lung through the formation of septal ridges.

253 his type of peptidoglycan is enriched in the septal ring as a product of catalysis by cell-wall amida

254 synthesis by PBP2b and positively regulates septal ring closure through its interactions with StkP-P

255 or depletion of GpsB prevents closure of the septal ring that in itself is PBP2x-dependent.

256 proteins FtsA and EzrA move out from mature septal rings coincident with MapZ rings early in cell di

257 eak systolic septal mitral annular velocity (Septal S') indicating poorer left function was associate

258 f-SEP -82 to -99) compared with anterior and septal segments (-65 to -79), whereas the reverse patter

259 tra-alveolar hemorrhages, extensive alveolar septal sequestration of bacteria and neutrophils, diffus

260 , related to invasive hemodynamics, leftward septal shift, and prolonged right ventricular systole.

261 to adverse pulmonary hemodynamics, leftward septal shift, and prolonged right ventricular systole.

262 n fraction patients 1 year after interatrial septal shunt device implantation.

263 y the major autolysin LytA and occurs at the septal site.

264 nferior-strain, -8.3% versus -9.9%; P<0.001; septal-strain, -9.1% versus -10.0%; P<0.001).

265 t echocardiography for selecting the correct septal (sub)branch; and 4) use of appropriate amounts of

266 ical VT: 12.5%) was attributed to intramural septal substrate in 13 of 18 patients (72%).

267 eeding, aortic and mitral valve surgery, and septal surgery increased the odds of RAO.

268 ed treadmilling, the spatial distribution of septal synthesis and the molecular composition and ultra

269 hesis machinery but do not limit the rate of septal synthesis.

270 nge in T1 time was not significant (Baseline septal T1 1277.4 ms, follow up 1271.5 p = 0.504).

271 diverting the antibiotic away from critical septal targets using CM anionic phospholipid redistribut

272 le range, 23-38 years) and more interlobular septal thickening and mediastinal lymphadenopathy on com

273 dation in nine of 14 (64%), and interlobular septal thickening in two of 14 (14%).

274 tributes to the impaired alveolarization and septal thickening observed in BPD.

275 Moreover, we also observed septal thickening, decreased alveolar air space total vo

276 f multifocal opacity and smooth interlobular septal thickening, possibly with small effusions, but wi

277 diastolic velocity in the LV correlated with septal thickness (R = 0.66; P = .01).

278 z-score difference = -0.64; p = 0.01) as was septal thickness (z-score difference = -0.93; p = 0.001)

279 In multivariable models (controlling for septal thickness and log-transformed N-terminal brain-ty

280 Mean maximal septal thickness was 19.0+/-3.9 mm, and total volume of

281 Mean alveolar septal thickness was greater in AMR patients than in con

282 Septal thickness was not significantly different between

283 -exposed group, LV mass and LV end-diastolic septal thickness were lower whereas LV contractility and

284 ifferentiation into another cell type during septal thinning have been proposed.

285 tion that the AMF lineage is depleted during septal thinning through a phagocytic process provides a

286 Mutant septal tips were stunted, lacked elastin-positive tips,

287 pEF (n=41) contrasted with right ventricular septal tissue from patients with HF with reduced ejectio

288 DNA extracted from cardiac interventricular septal tissue of 30 male HF patients encompassing causes

289 e rhythmicity of their firing decreases from septal to temporal termination of individual axons.

290 RV mechanical synchrony improved: septal-to-lateral RV mechanical delay decreased (P<0.001

291 re not atrioventricular pathways because the septal VA interval during tachycardia was <70 ms in 3, 1

292 Consistently, chemogenetic inhibition of septal vGAT neurons increased food intake.

293 roposed to have a specific catalytic role in septal wall synthesis.

294 M: -0.9+/-0.4 mm, P=0.017), interventricular septal wall thickness, posterior wall thickness, and rel

295 uides and regulates the inward growth of the septal wall.

296 This study aimed to evaluate whether septal widening could represent an "alert" signal for AM

297 mandatory to confirm the potential value of septal widening in the multidisciplinary approach of AMR

298 lesions conventionally associated with AMR, septal widening may represent an "alert" signal to look

299 Septal widening was a frequent, striking histological fe

300 Unexpectedly septal widening was the only histological change detecte