ライフサイエンスコーパス: hilar

1 Bilateral hilar (18)F-FDG-avid foci are often noted on PET studies

2 y-one patients with the finding of bilateral hilar (18)F-FDG-avid foci underwent a staging-only PET s

3 Thirty-nine IPNBs were identified in hilar (23/144), intrahepatic (4/86), and distal (12/113)

4 , cerebrospinal fluid (CSF) pleocytosis, and hilar adenopathy more frequently than NMOSD (p < 0.05);

5 evidence of supraclavicular or contralateral hilar adenopathy.

6 s in hippocampal mossy fiber synapses of the hilar and CA3 regions.

7 Complex renal tumors, such as hilar and endophytic lesions, have also been performed r

8 ity, lobular ground-glass opacification, and hilar and intercostal systemic collaterals were more pre

9 ITPR3 expression was increased in both hilar and intrahepatic CCA samples as well as in CCA cel

10 ion is the primary modality of treatment for hilar and intrahepatic cholangiocarcinoma (HCCA-ICCA).

11 A than in DSA, whereas the visibility of the hilar and intrarenal vessels was significantly worse (P

12 measuring 4.7 cm as well as several enlarged hilar and ipsilateral mediastinal lymph nodes.

13 gnostic performance of MR imaging in staging hilar and mediastinal lymph nodes in NSCLC on both a per

14 eedle aspiration (EBUS-TBNA) biopsies of the hilar and mediastinal lymph nodes, but the feasibility a

15 ed our hospital for examination of bilateral hilar and mediastinal lymphadenopathy.

16 ck-propagation aNN can be trained to predict hilar and mediastinal nodal involvement with greater acc

17 monkeypox antigen was detected in the lung, hilar and submandibular lymph nodes, spleen, and colon.

18 reased biopsy success rates for pretracheal, hilar, and high pretracheal adenopathy.

19 group and lung parenchymal, airway, pleural, hilar, and mediastinal abnormalities systematically revi

20 ide Y-containing interneurons in the dentate hilar area play an important role in inhibiting the acti

21 ition is caused by cholinergic activation of hilar astrocytes, which provide glutamatergic excitation

22 neurons, as well as a small number of mature hilar astrocytes.

23 HEGCs were much more likely to have a hilar basal dendrite than normotopic granule cells.

24 lity, including ectopic location, persistent hilar basal dendrites (HBDs), and mossy fiber sprouting.

25 s labeled by injecting RV after SE displayed hilar basal dendrites and ectopic migration, but not spr

26 SE revealed normally located DGCs exhibiting hilar basal dendrites and mossy fiber sprouting (MFS) wh

27 could explain the role of granule cells with hilar basal dendrites in contributing to hyperexcitabili

28 locarpine-epileptogenesis exhibited aberrant hilar basal dendrites.

29 Temoporfin-PDT can safely be delivered to hilar bile duct cancer patients and results in prolonged

30 n 71 [range 47-88] years) with nonresectable hilar bile duct cancer were treated with T-PDT (median 1

31 ves palliation and survival in nonresectable hilar bile duct cancer.

32 patients and results in prolonged patency of hilar bile ducts, a trend for longer survival time, and

33 the SE-experienced rat, excitatory drive to hilar border inhibitory interneurons is weakened through

34 produced a greater depression of GC input to hilar border interneurons in SE-experienced rats than in

35 s (GCs), perforant path, and CA3 inputs onto hilar border interneurons of the dentate gyrus were exam

36 yrus, often hundreds of micrometers from the hilar border, in the lucidum and radiatum layers.

37 GluR) modulation of glutamatergic input onto hilar-border interneurones and its regulation of feedbac

38 le cell layer and hilus combined, and 33% of hilar calretinin-positive cells.

39 e frequently in patients with lower lobe and hilar cancers combined compared with upper lobe cancers

40 posterior margin of the inferior vena cava (hilar-caval line) on lateral radiographs; this line corr

41 ted over (n = 66) or anterior to (n = 2) the hilar-caval line.

42 ts with operatively confirmed stage I and II hilar CCA in 1993.

43 n for patients with localized, node-negative hilar CCA.

44 h survival after resection for patients with hilar CCA.

45 was first used in patients with unresectable hilar CCAs, these methods have yet to reach broad applic

46 al, and molecular profile similar to that of hilar CCs (from mucin-producing cholangiocytes), whereas

47 nd molecular features of 85 resected CCs (14 hilar CCs [so-called Klatskin tumor], 71 intrahepatic CC

48 Immunoreactivity was similar in muc-ICCs and hilar CCs and in mixed-ICCs and CLCs.

49 and MUC1 were significantly up-regulated in hilar CCs and muc-ICCs compared with mixed-ICCs and CLCs

50 Clinicopathologically, muc-ICCs and hilar CCs showed a predominantly (peri-)hilar location,

51 Hilar cell assemblies, identified by simultaneous triple

52 promoters, and prevented kainic acid-induced hilar cell death.

53 -) mice showed a unique pattern of selective hilar cell loss (i.e., endfolium sclerosis), which so fa

54 planted animals produced similarly extensive hilar cell loss and immediate granule cell disinhibition

55 tide Y mRNA were compared with the degree of hilar cell loss determined by immunohistochemistry again

56 nterneurones occurs in proportion to overall hilar cell loss, and therefore the hypothesis of a selec

57 onsistently abolished after extensive (>85%) hilar cell loss.

58 Hilar cells are often among the first lost in hippocampa

59 s and presynaptic burst discharges, allowing hilar cells to respond over a large dynamic range of inp

60 erneurones with respect to the non-GABAergic hilar cells, i.e. the mossy cells.

61 from the decrease in the total population of hilar cells, indicating no preferential survival of inte

62 Sixty-five patients with unresectable hilar cholangiocarcinoma (CCA) have undergone orthotopic

63 de (LN) assessment after liver resection for hilar cholangiocarcinoma (HC) is still controversial, an

64 erged as a promising option for unresectable hilar cholangiocarcinoma (hCCA).

65 ntrahepatic cholangiocarcinoma (IH; n = 23), hilar cholangiocarcinoma (Hilar; n = 54), gallbladder (G

66 of intrahepatic cholangiocarcinoma (ICC) and hilar cholangiocarcinoma (Klatskin tumors) is limited to

67 y resectable gallbladder cancer (n = 44) and hilar cholangiocarcinoma (n = 56) were prospectively eva

68 A total of 257 patients (144 hilar cholangiocarcinoma [HCCA] and 113 distal bile duct

69 umor extent, the proposed staging system for hilar cholangiocarcinoma accurately predicts resectabili

70 ts receiving endoscopic biliary drainage for hilar cholangiocarcinoma between September 1995 and Dece

71 The yield of laparoscopy is lower for hilar cholangiocarcinoma but can be improved by targetin

72 formed a review of the English literature on hilar cholangiocarcinoma from 1990 to 2007.

73 Between 1997 and 2004, 80 patients with hilar cholangiocarcinoma having surgery were reviewed.

74 ic resection in hepatocellular carcinoma and hilar cholangiocarcinoma improves survival.

75 urvival in patients with surgically resected hilar cholangiocarcinoma in a single institution over th

76 Hilar cholangiocarcinoma is a rare tumor with a poor pro

77 Hilar cholangiocarcinoma is an uncommon tumor with a poo

78 Endoscopic biliary drainage of hilar cholangiocarcinoma is controversial with respect t

79 SEMS insertion for the palliation of hilar cholangiocarcinoma offers higher technical and cli

80 s the majority of patients with unresectable hilar cholangiocarcinoma or gallbladder carcinoma, there

81 r the study period was compared with that of hilar cholangiocarcinoma patients (HCCA) seen during the

82 From 1985 to 2006, all patients with hilar cholangiocarcinoma referred to a tertiary surgical

83 Hilar cholangiocarcinoma remains a difficult challenge f

84 y gallbladder cancer and patients with T2/T3 hilar cholangiocarcinoma should undergo staging laparosc

85 ompares outcome after resection of papillary hilar cholangiocarcinoma to that of the more common nodu

86 uated endoscopic palliation in patients with hilar cholangiocarcinoma using self-expandable metallic

87 ogic, and survival data on all patients with hilar cholangiocarcinoma were analyzed.

88 For patients with early stage hilar cholangiocarcinoma which is unresectable or arisin

89 and bile-duct resection can be performed for hilar cholangiocarcinoma with acceptable mortality, thou

90 In patients with hilar cholangiocarcinoma, concomitant hepatic resection

91 In patients with hilar cholangiocarcinoma, long-term survival depends cri

92 ant therapy followed by liver transplant for hilar cholangiocarcinoma, placed in context with the mos

93 locally advanced but potentially resectable hilar cholangiocarcinoma, the yield of laparoscopy was g

94 ve and only potentially curative therapy for hilar cholangiocarcinoma.

95 section remains the mainstay of treatment of hilar cholangiocarcinoma.

96 herapy followed by liver transplantation for hilar cholangiocarcinoma.

97 ates after aggressive surgical resections of hilar cholangiocarcinoma.

98 t determinant of survival after resection of hilar cholangiocarcinoma.

99 between patients with gallbladder cancer and hilar cholangiocarcinoma.

100 lecystectomy), but only 25% in patients with hilar cholangiocarcinoma.

101 This bidirectional plasticity enables hilar circuitry to regulate the flow of information thro

102 experimental murine PGD models were studied: hilar clamp and orthotopic lung transplantation after pr

103 NETs were increased after either hilar clamp or OLT-PCI compared with surgical control su

104 However, hilar clamping also renders the entire kidney ischemic,

105 tial nephrectomies performed with or without hilar clamping for clinical stage T1b tumors.

106 The reviewed data show that foregoing hilar clamping for T1b tumors is not only feasible, but

107 ist between cholecystokinin (CCK)-expressing hilar commissural associational path (HICAP) cells and a

108 d intraoperative blood loss when compared to hilar controlled procedures.

109 m can be an effective alternative to classic hilar dissection in cases when the latter is difficult o

110 dated videoscopic guidance and a traditional hilar dissection without rib spreading.

111 Our results demonstrate that hilar ectopic DGCs preferentially synapse onto adult-bor

112 seizure frequency and (1) the percentage of hilar ectopic DGCs, (2) the amount of mossy fiber sprout

113 ic times before or after SE decreased MFS or hilar ectopic DGCs, supporting the RV labeling results.

114 Hilar ectopic GCs (EGCs) can potentially provide insight

115 Hilar ectopic granule cells (HEGCs) are hyperexcitable a

116 Together, these data indicate that hilar ectopic granule cells are postsynaptic to mossy fi

117 th recent physiological results showing that hilar ectopic granule cells from epileptic rats are more

118 Electron microscopy was used to study hilar ectopic granule cells that were located 20-40 micr

119 Stereological methods were used to measure hilar ectopic granule cells, mossy cells, mossy fiber sp

120 nificantly correlated with the generation of hilar ectopic granule cells, the number of mossy cells,

121 es with the somata and proximal dendrites of hilar ectopic granule cells.

122 In the pilocarpine mTLE model, hilar-ectopic DGCs arise as a result of an aberrant chai

123 ws abnormal dispersion and the appearance of hilar-ectopic DGCs.

124 ntate gyrus and increased Dab1 expression in hilar-ectopic neuroblasts.

125 Consistently, hilar EGC and GC layer GCs had similar dendritic lengths

126 ensional analysis revealed that, remarkably, hilar EGC dendrites often extended along the longitudina

127 However, hilar EGC dendrites were topologically more complex, wit

128 efferent output, could help explain why the hilar EGC population could impair DG function.

129 Axonal reconstruction demonstrated that hilar EGCs contributed to mossy fiber sprouting.

130 tively analyzed the structural morphology of hilar EGCs from adult male rats several months after pil

131 Additionally, hilar EGCs that develop after SE may contribute to epile

132 Hilar EGCs were physiologically identified in slices, in

133 A chest x-ray showed bilateral hilar enlargement, thickening of the right paratracheal

134 study of patients with cancer with bilateral hilar foci on 1 or 2 sequential (18)F-FDG PET studies be

135 ntial and EPSC frequencies were increased in hilar GABA neurons from slices ipsilateral to the injury

136 excitatory synaptic activity was detected in hilar GABA neurons ipsilateral to the injury after gluta

137 s suggest that excitatory drive to surviving hilar GABA neurons is enhanced by convergent input from

138 short period of time prevented age-dependent hilar GABAergic interneuron decline and cognitive defici

139 with PB for 6 weeks prevented age-dependent hilar GABAergic interneuron decline and learning and mem

140 c mice; eliminating endogenous Tau prevented hilar GABAergic interneuron loss and the learning and me

141 n neurotoxic apoE4 fragment transgenic mice, hilar GABAergic interneuron loss was even more pronounce

142 n (KI) mice had an age-dependent decrease in hilar GABAergic interneurons that correlated with the ex

143 poE4-KI mice had an age-dependent decline in hilar GABAergic interneurons that correlated with the ex

144 in (KI) mice had an age-dependent decline in hilar GABAergic interneurons that correlated with the ex

145 causes age- and Tau-dependent impairment of hilar GABAergic interneurons, leading to learning and me

146 group, a trend towards increased numbers of hilar GAD cells was observed, even over and above that o

147 ed to test for monosynaptic connections from hilar GPHNs to granule cells.

148 ules did not arise directly from preexisting hilar IHBDs.

149 s, which provide glutamatergic excitation of hilar inhibitory interneurons.

150 This rewiring of circuitry regulating hilar inhibitory neurons may reflect an important compen

151 sionally reconstructed 216-microm-long spiny hilar interneuron axon segment in the outer third of the

152 The numbers of hilar interneurones expressing somatostatin mRNA and neu

153 The percentage decrease in the number of hilar interneurones labelled with either GAD67 or parval

154 ntrast, SOMIs with axon in the hilus, termed hilar interneurons (HILs), provide perisomatic inhibitio

155 ells and excitability of surviving GABAergic hilar interneurons 8-13 weeks after cortical contusion b

156 nerability of a particular subset of dentate hilar interneurons after prolonged SE.

157 ta-estradiol in ovariectomized rats protects hilar interneurons against seizure-induced injury, inclu

158 Hilar interneurons also show synapse specificity and pre

159 We also observed that hilar interneurons and associated NG2(+) cells are simil

160 utamatergic and monosynaptically excite both hilar interneurons and mossy cells.

161 Although many somatostatin-positive hilar interneurons effectively transported FG from the d

162 erefore, in the outer molecular layer, spiny hilar interneurons form synaptic contacts that appear to

163 eneration and tauopathy occurred earliest in hilar interneurons in apoE4 fragment transgenic mice; el

164 of the transplanted neurons with endogenous hilar interneurons in mice without TLE.

165 tions and synaptic connections made by spiny hilar interneurons labeled with biocytin in gerbils in v

166 Some of hilar interneurons of the dentate gyrus express neuropep

167 , in all groups, we observed a population of hilar interneurons that were CHT-immunoreactive.

168 connectivity may be mechanisms for surviving hilar interneurons to inhibit more granule cells and com

169 gnaling events that render somatostatinergic hilar interneurons vulnerable to SE-induced cell death.

170 s of NPY expression in the cortex, CA1, CA3, hilar interneurons, and granule cells of the dentate gyr

171 erneurons and suggest that the loss of spiny hilar interneurons, as occurs in temporal lobe epilepsy,

172 ilar mossy cells, but not peptide-containing hilar interneurons, indicating that mossy cells are the

173 t-born granule cells establish synapses with hilar interneurons, mossy cells and CA3 pyramidal cells

174 n this region, glutamatergic mossy cells and hilar interneurons, or the organization of local circuit

175 populations of dentate gyrus mossy cells and hilar interneurons.

176 of their intralamellar connections are onto hilar interneurons.

177 nd in vulnerable somatostatin-immunoreactive hilar interneurons.

178 estradiol enhances NPY expression within the hilar interneurons.

179 ve cohort of patients with bile duct cancer (hilar, intrahepatic, or distal) was reviewed, and those

180 Hilar IPSPs have low failure rates, are blocked by the G

181 The dominant positive polarity of hilar LFPs was only produced by the synchronous activati

182 An in vivo murine hilar ligation model of IR injury was used, in which lef

183 and hilar CCs showed a predominantly (peri-)hilar location, smaller tumor size, and more lymphatic a

184 on, and proliferative responses of pulmonary hilar lymph node CD4 T cells to autologous lung extracts

185 of 120 days or less (HR, 2.6; P = 0.01) and hilar lymph node invasion (HR = 2.2; P = 0.03), but not

186 tments (bronchoalveolar lavage, lung tissue, hilar lymph node) at AAD and LIT; systemic compartments

187 ed from T lymphocytes in blood, airways, and hilar lymph node, with responses predominantly localized

188 ells in the bronchoalveolar lavage (BAL) and hilar lymph nodes (HLN) at the resolution stage of this

189 t been characterized in cells from pulmonary hilar lymph nodes (PHLN).

190 ed enlarged hyperattenuating mediastinal and hilar lymph nodes and edema of mediastinal fat.

191 of hyperdense non-calcified mediastinal and hilar lymph nodes, known as "brilliant lymph nodes", com

192 ease, nor were there enlarged mediastinal or hilar lymph nodes.

193 ge II disease, that is, metastatic spread to hilar lymph nodes.

194 ulmonary nodules (31.4%), mediastinal and/or hilar lymphadenopathy (23%), mass-like consolidation (17

195 ess with incipient pneumonia, pleuritis, and hilar lymphadenopathy.

196 cic tuberculosis would be based primarily on hilar lymphadenopathy.

197 dule (n = 1), multiple nodules (n = 1), or a hilar mass (n = 1).

198 raphy (CT) angiogram, there is a large right hilar mass and enlarged mediastinal lymph nodes but no p

199 n a marked decrease in the size of the right hilar mass and mediastinal lymph nodes.

200 tients underwent 155 liver transplants using hilar mass clamping.

201 nction; an ultrasound examination revealed a hilar mass, with hydronephrosis in five and stenosis of

202 symptomatic, and imaging typically reveals a hilar mass.

203 diagnosed in 5 of 77 patients (6.5%), while hilar/mediastinal lymphadenopathy was found in 25 of 76

204 N1 hilar metastases were diagnosed in 8 patients (12.9%) be

205 Excitatory hilar mossy cells (MCs) in the dentate gyrus receive inp

206 -spiking interneurons, a burstiness code for hilar mossy cells and a synchrony code at long time scal

207 both p11 and SMARCA3 are highly enriched in hilar mossy cells and basket cells.

208 In addition to the dentate hilar mossy cells and CA3 pyramidal cells shown previous

209 Whereas hilar mossy cells and CA3 pyramidal cells were FG-labele

210 nt vulnerability of dendritically projecting hilar mossy cells and interneurons and the relative resi

211 lutamate receptor subunit 2 (GluR2)-positive hilar mossy cells and peptide-containing interneurons in

212 pothesis in light of reports that excitatory hilar mossy cells are not consistently vulnerable and in

213 Longitudinal projections of excitatory hilar mossy cells could be viewed as antithetical to lam

214 However, whether it is the disappearance of hilar mossy cells from the dentate gyrus circuitry after

215 reduces evoked IPSC amplitude recorded from hilar mossy cells in the rat dentate gyrus through a pre

216 eedback inhibition of GABAergic afferents to hilar mossy cells is governed by a complex relationship

217 The ADP observed in hilar mossy cells is produced by the opening of a Na(+)

218 We show that hilar mossy cells provide initial glutamatergic synapses

219 cells converge on the hilus, and excitatory hilar mossy cells redistribute these signals back to gra

220 ncy of miniature IPSCs (mIPSCs)recorded from hilar mossy cells without altering event amplitude, area

221 ipal cells, including dentate granule cells, hilar mossy cells, and hippocampal pyramidal cells, were

222 in GCs than in fast-spiking interneurons and hilar mossy cells, and is amplified in CA3 pyramidal cel

223 6 mice destroyed most GluR2-positive dentate hilar mossy cells, but not peptide-containing hilar inte

224 Hilar mossy cells, in particular, are thought to show dr

225 re, after epileptogenic treatments that kill hilar mossy cells, mossy fiber sprouting does not simply

226 min, and calretinin interneurons, as well as hilar mossy cells, new adult-born neurons, and recently

227 n null mice and an increase in the number of hilar mossy cells.

228 noma (IH; n = 23), hilar cholangiocarcinoma (Hilar; n = 54), gallbladder (GB; n = 32), and distal bil

229 ely to modulate neuronal excitability in the hilar network, and further reveal a mechanism that could

230 le cell discharges always produced extensive hilar neuron degeneration and immediate granule cell dis

231 ings are consistent with the hypotheses that hilar neuron loss and ectopic granule cells might contri

232 The degree of hilar neuron loss and mossy fiber sprouting correlated s

233 llar inhibition was intact in rats with <40% hilar neuron loss but was consistently abolished after e

234 ificantly affect granule cell proliferation, hilar neuron loss, or generation of ectopic granule cell

235 r of neuronal nuclear antigen-immunoreactive hilar neurones.

236 es revealed substantial loss of GFP-positive hilar neurons (GPHNs) but increased GFP-positive axon le

237 ptic barrages triggered persistent firing in hilar neurons (hilar up-states).

238 ons were among the many retrogradely labeled hilar neurons 2.5-4.5 mm longitudinally.

239 Population responses recorded in hilar neurons accurately encoded stimulus identity.

240 wed the identification of a subpopulation of hilar neurons known as mossy cells (MCs) as a prominent

241 Patterns of synaptic input onto dentate hilar neurons predicted which of four pathways were stim

242 e gyrus (DG) are a major group of excitatory hilar neurons that are important for regulating activity

243 ry, including an extensive bilateral loss of hilar neurons throughout the hippocampal longitudinal ax

244 ause the total number of NeuN-immunoreactive hilar neurons was unaffected, the decline observed with

245 In addition, surviving NPY-immunoreactive hilar neurons were distributed preferentially in the sup

246 By contrast, other types of hilar neurons were less strongly depolarized by bath app

247 in SGCs and synaptic barrages in downstream hilar neurons without blocking fast synaptic transmissio

248 activation on the intrinsic excitability of hilar neurons.

249 lls evoke EPSPs with high failure rates onto hilar neurons.

250 rticular prominence is the loss of GABAergic hilar neurons.

251 ivation was repressed in STEP-immunoreactive hilar neurons.

252 of the hippocampal CA3 pyramidal and dentate hilar neurons.

253 dentate gyrus despite loss of immunopositive hilar neurons.

254 were identified by the loss of Nissl-stained hilar neurons.

255 excitability, and control aspirations of the hilar neuropil or of interneurons in the presence of GAB

256 tion, we performed patch-clamp recordings on hilar NG2(+) cells and interneurons between 3 and 21 pos

257 We first observed that hilar NG2(+) cells exhibit spontaneous glutamatergic EPS

258 Hilar nodes and parenchymal lung tissue were processed a

259 way from the staple line, and in ipsilateral hilar nodes.

260 flammation and Th2 cytokines in restimulated hilar nodes.

261 her, we show that beta-estradiol upregulates hilar NPY and that this leads to enhancement in dentate

262 Hilar NPY neurons showed modest spike frequency adaptati

263 ting lymph node metastases in lower lobe and hilar NSCLC compared with upper lobe NSCLC.

264 eatography (ERCP) in management of malignant hilar obstruction (MHO) remains unclear.

265 obular enlargement in the liver secondary to hilar obstruction.

266 ry stenting (HR 3.274, P=0.019), distal (non-hilar) obstruction of the bile ducts (HR 3.711, P=0.008)

267 r and more complex tumors including those in hilar or central locations, in kidneys with multiple mas

268 However, hilar path activity could be seen after LTP, with or wit

269 The hilar pathology was often associated with hepatic artery

270 ells and among somatostatin (SOM)-containing hilar perforant path-associated (HIPP) interneurons.

271 Hilar-perforant-path-associated interneurons (HIPP cells

272 gh excitatory mossy cells of the hippocampal hilar region are known to project both to dentate granul

273 It is suggested that the dentate gyrus and hilar region in the hippocampus perform memory selection

274 so was observed in large bile ducts from the hilar region of primary sclerosing cholangitis patients.

275 microglial cells and their processes in the hilar region of the dentate gyrus of adult Sprague-Dawle

276 ed in the subventricular zone but not in the hilar region of the dentate gyrus.

277 tostatin mRNA and neuropeptide Y mRNA in the hilar region of the hippocampal formation of patients wi

278 ived significant synaptic input from the CA3/hilar region, especially under conditions of experimenta

279 ients treated for targets within the lung or hilar region.

280 e found to be exclusively located within the hilar region.

281 of symmetric and mild uptake limited to the hilar regions that are stable on 2 sequential PET studie

282 In AA rats, sympathetic nerve density in the hilar regions, where NA nerves enter the spleen, was inc

283 mprove behavioral performance fully restored hilar SOM expression in aged, memory-impaired rats.

284 ether, these findings suggest that surviving hilar somatostatin interneurons enlarge, extend dendrite

285 ble among animals, but was as high as 96% of hilar somatostatin-positive interneurons, 84% of parvalb

286 In area CA3, repetitive hilar stimuli frequently evoked multiple population spik

287 Classic dissection of the hilar structures during the hepatectomy portion of the l

288 In such cases, clamping of the hepatic hilar structures en mass can be an effective alternative

289 rm the hepatectomy with mass clamping of the hilar structures was an intraoperative judgment made whe

290 surface of the kidney, as well as posterior hilar structures.

291 Intralamellar hilar synapses appear to function primarily by integrati

292 ially inhibit mossy cells; 81% of inhibitory hilar synapses are onto mossy cells.

293 n the lung adjacent to a central mediastinal/hilar thoracic mass were excluded (range,.59 to.91).

294 Thus, restricted hilar transplantation of inhibitory interneurons restore

295 Overlap in the pathogenesis of GB and Hilar tumors was suggested.

296 1b tumors and more complex tumors, including hilar tumors, central tumors or tumors in solitary kidne

297 Hilar up-states triggered functional inhibition in granu

298 riggered persistent firing in hilar neurons (hilar up-states).

299 scarring of the hilum (n = 137) or extensive hilar varices (n = 18) were encountered.

300 The expression profiles of GB and Hilar were more similar to each other than either was to