ライフサイエンスコーパス: NSC

1 NSC limitation, immediate temperature, accumulated heat,

2 NSCs decreased from L to LD to D seedlings.

3 NSCs in the dentate gyrus (DG(have enigmatic elaborated

4 uiescent NSCs become activated prior to G(0) NSCs.

5 thdrawal of Cup/Rap, proliferation of type 1 NSCs and dendritic spine densities of adult-born neurons

6 Specifically, radial glia-like type 1 NSCs were shifted from a proliferative state to a mitoti

7 cued the self-renewal defect of Sox2-ablated NSCs.

8 In addition, NSC might provide a useful theoretical framework under w

9 orso-ventral axis, division pattern of adult NSCs, maturation time plan of newborn neurons, and ongoi

10 ocytes to regulate the key behavior of adult NSCs.

11 After NSC divisions in vitro, midbody remnants are more often

12 t intermediate signal transducer that allows NSCs to sense and respond to extracellular stiffness cue

13 Although NSC might not apply to all brain areas (for example, mot

14 r 1) negatively regulates niche capacity and NSC number in the adult ventricular-subventricular zone

15 obeads for the coincident delivery of EC and NSC as a means of enhancing appropriate NSC quiescence a

16 We demonstrate that EC and NSC co-encapsulation maintained NSC quiescence, enhanced

17 in mice, increasing the numbers of NSCs and NSC units.

18 ns, in regulating neurogenic niche cells and NSCs.

19 For the DADA2-SSN approach, NSC numbers decreased from 3.5-fold to 3-fold overestima

20 and NSC as a means of enhancing appropriate NSC quiescence and survival during transplantation into

21 of cortical development and gets induced as NSCs begin to differentiate.

22 trends, there was no clear trade-off between NSC storage and growth suggesting that both were similar

23 ulatory neurogenic mediators are 'sensed' by NSCs.

24 , is also readily and selectively uptaken by NSCs and reduces their proliferation, which might explai

25 Despite non-structural carbohydrate (NSC) importance for tree productivity and resilience, li

26 (total biomass, nonstructural carbohydrates (NSC) and secondary metabolites (SM)) in well-watered Nor

27 e importance of nonstructural carbohydrates (NSC) for growth and survival in woody plants, we know li

28 the xylem store nonstructural carbohydrates (NSC), providing reserves of energy that fuel woody peren

29 used a dynamic non-structural carbohydrates (NSC) model (FORCCHN2) that couples leaf development and

30 consume stored nonstructural carbohydrates (NSCs).

31 phy, enable the control of neural stem cell (NSC) differentiation and neurite outgrowth.

32 cal regulator of mammalian neural stem cell (NSC) fate and a bona fide human disease gene in congenit

33 ell types to regulation of neural stem cell (NSC) homeostasis and maturation of adult-born DGCs.

34 abundant in the early-born neural stem cell (NSC) lineage and regulates neuronal morphology.

35 In Drosophila neural stem cell (NSC) lineages, excessive Notch signalling results in sup

36 ion factor is critical for neural stem cell (NSC) maintenance and brain development.

37 ne play a critical role in neural stem cell (NSC) maintenance, quiescence and survival.

38 Regulation of adult neural stem cell (NSC) number is critical for lifelong neurogenesis.

39 for the maintenance of the neural stem cell (NSC) pool in the adult subventricular zone (SVZ) niche b

40 ancing rates and timing of neural stem cell (NSC) proliferation, neurogenesis and cell death.

41 is required for embryonic neural stem cell (NSC) proliferation.

42 Increased neural stem cell (NSC) quiescence is a major determinant of age-related re

43 d an unexpected ability of neural stem cell (NSC) therapies to provide neurotrophic support and inhib

44 described in terms of the neural stem cell (NSC)/carnitine malnutrition hypothesis, that an unapprec

45 imed to evaluate UPE from neural stem cells (NSC) during their serial passaging and differentiation.

46 etic mouse model in which neural stem cells (NSC) of the subventricular zone (SVZ) were temporarily e

47 Transplanted human neural stem cells (NSC) that have the potential to differentiate into funct

48 nsition of neural stem and progenitor cells (NSCs) from proliferative to differentiative divisions to

49 cy of allogenic/intrinsic neural stem cells (NSCs) after spinal cord injury is severely compromised b

50 ZIKV-host interactome in neural stem cells (NSCs) and found that Dicer is specifically targeted by t

51 demonstrating that adult neural stem cells (NSCs) are a cell of origin of glioblastoma.

52 Neural stem cells (NSCs) are multipotent progenitors that are responsible f

53 uronal differentiation of neural stem cells (NSCs) by suppressing cytoskeletal contractility.

54 multiple sclerosis (MS), neural stem cells (NSCs) can replace damaged oligodendrocytes if the local

55 n contains few niches for neural stem cells (NSCs) capable of generating new neurons, whereas other r

56 campal dentate gyrus (DG) neural stem cells (NSCs) continuously undergo proliferation and differentia

57 mechanisms that regulate neural stem cells (NSCs) during aging, focusing on the effect of metabolism

58 veloped highly expandable neural stem cells (NSCs) from HESCs and iPSCs that artificially express the

59 Neural stem cells (NSCs) generate neurons and glial cells throughout embryo

60 Neural stem cells (NSCs) generate neurons throughout life in the mammalian

61 f projection neurons from neural stem cells (NSCs) in a cell-autonomous manner, altering postnatal co

62 Quiescent neural stem cells (NSCs) in the adult brain are regenerative cells that cou

63 Here, we show that neural stem cells (NSCs) in the adult mouse hippocampus actively transcribe

64 Neural stem cells (NSCs) in the dentate gyrus (DG) reside in a specialized

65 Neural stem cells (NSCs) in the developing and postnatal brain have distinc

66 ent manner, especially in neural stem cells (NSCs) in which the expression of opioid receptors and en

67 an integral component of neural stem cells (NSCs) niches.

68 rt a dramatic drop in the neural stem cells (NSCs) number in the aging murine brain. We find that thi

69 t inhibition of OxPhos in neural stem cells (NSCs) or tumours in the Drosophila brain not only decrea

70 tential, radial glia-like neural stem cells (NSCs) proliferation and differentiation, migration, and

71 f Zika virus infection in neural stem cells (NSCs) remains elusive.

72 Adult neural stem cells (NSCs) reside in specialized niches, which hold a balance

73 e two sites where adult neuronal stem cells (NSCs) reside.

74 ze and structure requires neural stem cells (NSCs) to divide with tight temporal and spatial control

75 50 primary tumors, and 10 neural stem cells (NSCs) to identify essential super-enhancer (SE)-associat

76 The ability of neural stem cells (NSCs) to transit between quiescence and proliferation is

77 we demonstrate that adult neural stem cells (NSCs) utilize aggresomes to recover from disrupted prote

78 logically primed stage in neural stem cells (NSCs), reflected by altered chromatin accessibility.

79 of differentiating adult neural stem cells (NSCs).

80 by the cell divisions of neural stem cells (NSCs).

81 nhibited proliferation of neural stem cells (NSCs).

82 euroepithelium to produce neural stem cells (NSCs).

83 iptomics of NSCs indicate that aging changes NSCs minimally.

84 nce grouping into network sequence clusters (NSCs).

85 binds ACVR1 to form a non-signaling complex (NSC).

86 As a conclusion, NSC have UPE-properties and the intensity is increased b

87 As a consequence, NSCs fail to undergo terminal differentiation, leading t

88 nment but is unlikely to spatially constrain NSC storage.

89 rial biophysical cue sensor array to control NSC behavior via electrical stimuli can be potentially u

90 roteasome machinery to aggresomes to control NSC proteostasis during quiescence exit.

91 ind that p53-dependent apoptosis of cortical NSCs accounts for most of the microcephaly, but that the

92 R levels in doublecortin expressing (DCX(+)) NSC progenies in the rat DG.

93 s that ultimately govern stiffness-dependent NSC fate commitment are not fully understood.

94 ange chromatin interactions in brain-derived NSCs.

95 Grafting embryonic spinal cord-derived NSCs or injury alone served as 2 controls.

96 gnificant metabolic component in determining NSC vulnerability to derangements in their self-renewal

97 Although proliferation of these adult DG NSCs has been implicated in opiate dependence, whether N

98 rdially to mice is selectively uptaken by DG NSCs within a minute, via the vessel-associated apical p

99 that conditional overexpression of MOR in DG NSCs under a doxycycline inducible system leads to facil

100 rs differentiation and dendritogenesis of DG NSCs and investigate the possibility that these alterati

101 mu-opioid receptor (MOR) is expressed on DG NSCs and that MSA leads to a two-fold elevation of endog

102 favorable substrate stiffness for directing NSC differentiation.

103 y a single-cell material-EMSCs for directing NSC differentiation.

104 The newly-discovered NSC-BV communication route explains how circulatory neur

105 We discuss NSC transplantation as a promising therapy for P-MS, ela

106 p locus and induces Dap expression in dorsal NSCs, resulting in G(0) arrest, while more ventral NSCs

107 f neurons with the characteristics of dorsal NSCs in vivo.

108 blasts (NBs), one of the two main Drosophila NSC identities.

109 MB neuroblasts are a subset of Drosophila NSCs that generate neurons important for memory and lear

110 Even without drought, NSC depletion impaired osmoregulation and turgor mainten

111 ion timing and midbody remnants in embryonic NSCs may influence proper brain growth and structure.

112 o imprecision in the integration of emerging NSCs into the front.

113 We find that emerging NSCs remain epithelial and apically constrict before div

114 ons, supporting and guiding later emigrating NSCs (Sox9+) through multiple transient zones prior to c

115 sulation maintained NSC quiescence, enhanced NSC viability, and facilitated NSC extravasation in vitr

116 ecific deletion of Ccn1 transiently enhanced NSC proliferation and reduced neuronal differentiation i

117 Although morphogens initially establish NSC positional identity in the neural tube, it is unclea

118 eventually returned to normal, the expanded NSC pool was maintained in the V-SVZ until old age.

119 Zfp488 expressing NSC derived oligodendrocytes are functional and can myel

120 nce, enhanced NSC viability, and facilitated NSC extravasation in vitro, as compared to NSC encapsula

121 We used two-photon microscopy and followed NSCs that were genetically labeled through conditional r

122 with chromatin is markedly reduced following NSC differentiation.

123 served E3 ubiquitin ligase, is essential for NSC reactivation (exit from quiescence).

124 tential of a biomimetic engineered niche for NSC delivery into the brain following neurological injur

125 igase (CRL4), are intrinsically required for NSC reactivation.

126 ng that both were similarly strong sinks for NSC.

127 ther signal through FOP-mutant ACVR1 or form NSCs with wild-type ACVR1.

128 level to ensure continuous neurogenesis from NSCs remains unknown.

129 nsider how new technologies may help harness NSCs' potential to restore healthy brain function during

130 4% neuronal differentiation of the harvested NSCs.

131 s, supporting the existence of heterogeneous NSC populations with diverse behavioral properties.

132 tudy shows that proliferation of hippocampal NSCs and synaptic connectivity of adult-born neurons are

133 ial of the young DG and suggests hippocampal NSCs as a critical reservoir enabling recovery from cata

134 ess of blood-borne substances to hippocampal NSCs.

135 Finally, we speculate how NSCs integrate niche-derived signals to govern their reg

136 Forced expression of Zfp488 gene in human NSCs led to the robust generation of OLs and suppression

137 We detect an age-dependent decrease in NSC O-GlcNAc levels coincident with decreased neurogenes

138 s reveal a role for beta-catenin dynamics in NSC fate decisions and may suggest a role for signal tim

139 , E(spl)mgamma was no longer extinguished in NSC progeny.

140 ification of genes and enhancers involved in NSC maintenance and neurodevelopmental disorders.

141 eins promote elimination of Ascl1 protein in NSC cultures.

142 furrow ingression and midbody abscission in NSCs within cortical explants.

143 y demonstrates that the miR-17-92 cluster in NSCs is critical for cognitive and behavioral function a

144 rs2 preferentially occupies DNA enhancers in NSCs, where it colocalizes broadly with NSC regulator SO

145 nked beta-N-acetylglucosamine (O-GlcNAc), in NSCs promotes a glial fate switch.

146 YAP), is critical for mechanotransduction in NSCs.

147 rough connections to the enhancer network in NSCs.

148 tion factor that increases susceptibility in NSCs and glioblastoma stem cells.

149 We present evidence that in NSCs Chi3l3 activates the epidermal growth factor recept

150 ely mimics human opiate addiction, increases NSC neuronal differentiation and promotes neuronal dendr

151 Cs and morphine treatment in vitro increases NSC neuronal differentiation and dendritogenesis, sugges

152 romoted effective regeneration by increasing NSCs proliferation/survival rates, restoring a nearly or

153 ial for long-term self-renewal of individual NSCs within the adult brain remains unclear.

154 ZIKV-infected NSCs show global dampening of miRNA production, includin

155 mmatory response compared to freely injected NSC.

156 n and fabrication of flexible interdigitated NSCs that rival state-of-the-art supercapacitors in perf

157 Here we test the contribution of intrinsic NSC apoptosis to brain size reduction in this lethal mic

158 ies confirm that EMSCs can promote intrinsic NSC neuronal differentiation and domesticating astrocyte

159 and increased neurogenesis of Pnky-knockout NSCs, as well as the developmental phenotypes of Pnky-de

160 re also observed in opioid receptor-knockout NSCs.

161 e ten-eleven translocation 1 (Tet1) knockout NSCs.

162 n of the miR-17-92 cluster in nestin lineage NSCs, we tested the hypothesis that the miR-17-92 cluste

163 that EC and NSC co-encapsulation maintained NSC quiescence, enhanced NSC viability, and facilitated

164 Drosophila Hippo pathway maintains NSC quiescence, but its regulation during brain developm

165 Mammalian NSCs in the embryonic cortex must maintain their polariz

166 In adult mammals, NSCs reside predominantly in a mitotically dormant, quie

167 1+) extensively targeted contacts to mitotic NSCs (Notch active), revealing a substrate for cell-cell

168 defective palmitoylation of BMPR1a modulates NSC function within the mouse brain, resulting in enhanc

169 entify proteins that are S-acylated in mouse NSCs and showed that bone morphogenic protein receptor 1

170 polarized furrowing and abscission in mouse NSCs are regulated differently at earlier and later stag

171 scission is accelerated in the Kif20b mutant NSCs.

172 ssion is slower in a subset of Kif20b mutant NSCs.

173 Accumulation of p53 in the nucleus of mutant NSCs at midbody stage suggests the possibility of a nove

174 In addition, Ars2 null NSCs can still transition into post-mitotic neurons, but

175 In oaks, NSC was explained by environment - values increasing for

176 to maintain 'operational' concentrations of NSC while investing newly-assimilated C into future surv

177 modifications of proteins in the context of NSC biology.

178 y of NSC that pushes more differentiation of NSC to the neurons.

179 NPs or mirror) affect the differentiation of NSC.

180 ther before nor after the differentiation of NSC.

181 We characterize the seasonal dynamics of NSC in relation to the aboveground phenology and tempora

182 Seasonal dynamics of NSC were synchronous between wood tissues from trunk, br

183 xcess Notch activity so that re-emergence of NSC properties occurs only in older progeny.

184 The AgNPs increases the UPE intensity of NSC that pushes more differentiation of NSC to the neuro

185 Mimicking an age-related loss of NSC O-GlcNAcylation in young mice reduces neurogenesis,

186 We found that the maintenance of NSC positional identity in the murine brain requires a m

187 criptional mechanisms for the maintenance of NSC quiescence and reveal a role for Id4 as a quiescence

188 vated apoptosis and defects in maturation of NSC midbodies, which mediate cytokinetic abscission.

189 modified earlier views on the mechanisms of NSC self-renewal and neurogenesis in the adult brain.

190 tor-mediated mechanism for C1q modulation of NSC behavior and show that modification of C1q receptor

191 Studying TRIM71 as a paradigm of NSC involvement in CH is a remarkable opportunity to bet

192 had almost identical levels and patterns of NSC variation in twigs, branches and trunks whereas pist

193 aloxone, were used during the early stage of NSC differentiation, increased neurogenesis was observed

194 n of Tet1 decreased during the late stage of NSC differentiation, morphine, but not naloxone, inhibit

195 or executive function areas) the success of NSC-based models, especially in sensory areas, warrants

196 UPE of NSC after the differentiation was significantly lower th

197 have microcephaly and elevated apoptosis of NSCs.

198 ified a mechanism regulating the behavior of NSCs and provided the framework to characterize dynamic

199 osed in which division-coupled conversion of NSCs into differentiated astrocytes restrict the stem ce

200 pillar array enhanced the differentiation of NSCs and efficiently regulated neuronal behavior, such a

201 cts of opioids during the differentiation of NSCs and provided additional insight on the complex func

202 e by preventing premature differentiation of NSCs into non-neurogenic astrocytes.

203 ile inhibiting astroglial differentiation of NSCs is not reported.

204 pre-mature activation and differentiation of NSCs without changing their neurogenic potential.

205 ts for promoting neuronal differentiation of NSCs, and meanwhile, inhibiting astrocyte overproliferat

206 troglial but not neuronal differentiation of NSCs.

207 Through intravital imaging of NSCs and their progeny, we identify a population of Gli1

208 is regulated to contain a specific number of NSCs remains unclear.

209 the cerebrospinal fluid to control number of NSCs within the SEZ.

210 ized niches, which hold a balanced number of NSCs, their progeny, and other cells.

211 entiation in mice, increasing the numbers of NSCs and NSC units.

212 Although proliferation of NSCs and neurogenesis seen in Ccn1 knockout mice eventua

213 s with decreased neurogenic proliferation of NSCs and upregulation of genes involved in immune proces

214 release supports neurogenic proliferation of NSCs through a dominant astrocyte-mediated glutamatergic

215 A shift of NSCs from a proliferatively-active state to mitotically-

216 Single-cell transcriptomics of NSCs indicate that aging changes NSCs minimally.

217 Once activated, however, young and old NSCs show similar proliferation and differentiation capa

218 ore emerging rejuvenating strategies for old NSCs.

219 by an increase in quiescence that makes old NSCs more resistant to regenerate the injured brain.

220 neutralize them increases activation of old NSCs during homeostasis and following injury.

221 ver, the effect of these biophysical cues on NSC behavior has not been fully elucidated.

222 ile phenology had a significant influence on NSC seasonal trends, there was no clear trade-off betwee

223 that MOR mediates the effect of morphine on NSC neuronal differentiation and maturation.

224 stem and land surface models all overpredict NSC storage.

225 We measured plant NSCs, osmotic and water potential, and transfer of (13)

226 Using RNA-sequencing of primary NSCs following decreased O-GlcNAcylation, we detected ch

227 ons of residing granule cells, proliferating NSCs and BrdU+ neurons in the dDG, whereas newborn neuro

228 ficantly reduced the number of proliferating NSCs and neuroblasts and neuronal differentiation in the

229 Importantly, EM networks propagated NSC depletion and its negative effects on water retentio

230 istinct subtypes of Drosophila FACS-purified NSCs and their differentiated progeny to dissect the epi

231 , to control the maintenance of quiescent (q)NSCs.

232 regulation of proteostasis during quiescent NSC activation.

233 s will require an understanding of quiescent NSC heterogeneities and regulation during normal physiol

234 We found that G(2)-quiescent NSCs become activated prior to G(0) NSCs.

235 s, a first step towards harnessing quiescent NSCs for therapeutic purposes.

236 binding protein Id4 is enriched in quiescent NSCs and that elimination of Id4 results in abnormal acc

237 We further show that quiescent NSCs are the main source of their local ECM, including t

238 It is hoped that quiescent NSCs could be activated therapeutically to contribute to

239 It is becoming apparent that quiescent NSCs exhibit heterogeneity in their propensity for activ

240 ression is also detected in the cultured rat NSCs and morphine treatment in vitro increases NSC neuro

241 generative decline underlying an age-related NSC fate switch.

242 us, we here identify long-term self-renewing NSCs that contribute to the generation of new neurons in

243 Thus, ependyma-derived CCN1 restricts NSC expansion in the adult brain to maintain the proper

244 thermore, spinal cord retransection below RN-NSC grafts partially eliminated the recovery in AD.

245 of 5-HT(2A) receptors with ketanserin in RN-NSC-grafted rats reduced resting mean arterial pressure

246 ecord cardiovascular parameters, grafting RN-NSCs restored resting mean arterial pressure to normal l

247 us-derived neural stem cells/progenitors (RN-NSCs) into a complete spinal cord transection lesion sit

248 Collectively, these data indicate that RN-NSCs grafted into a spinal cord injury site relay supras

249 Ray parenchyma fraction (RPF) and seasonal NSC dynamics were quantified for 12 conifers and three o

250 Stored NSC depletion may impair the regulation of plant water b

251 uence plant drought tolerance through stored NSC depletion.

252 ough EM to explore mechanisms linking stored NSCs to plant water balance regulation and identify pote

253 apacitors by preparing nano-supercapacitors (NSCs) with interdigital nanosized electrodes using focus

254 ve Notch signalling results in supernumerary NSCs causing hyperplasia.

255 ecification and cell division modes of V-SVZ NSCs, and draw comparisons with NSCs in the SGZ.

256 In contrast, once activated, Ascl1-targeted NSCs undergo limited proliferative activity before they

257 y, we identify a population of Gli1-targeted NSCs showing long-term self-renewal in the adult hippoca

258 We demonstrate that NSC storage depletion influences turgor maintenance inde

259 We review evidence that NSC might be employed by sensory areas to efficiently en

260 The conventional theory suggests that NSC reserves will increase over the growing season and d

261 We discovered recently that NSCs undergo quiescence in either G(0) or G(2) in the Dr

262 In addition, the NSC midbody maturation defects are not rescued by p53 de

263 rable analog of naloxone, did not affect the NSC differentiation.

264 first evidence for a biological role for the NSC in vivo and pave the way for further exploration of

265 ins, we demonstrate that failure to form the NSC in FOP results in more severe disease pathology.

266 ins that activate ACVR1B but cannot form the NSC with ACVR1.

267 AgNPs significantly increased the UPE of the NSC compared to the control group before and after the d

268 The UPE of the NSC in the sixth subculturing passage was significantly

269 of EGFR signaling prevented expansion of the NSC population observed in CCN1 deficient mice.

270 s been studied extensively, the roles of the NSC remain unexplored.

271 pave the way for further exploration of the NSC's physiological role in corresponding knock-in mice.

272 To explore the role of the NSC, we generated 'agonist-only' Activin A muteins that

273 One major prediction of the NSC/carnitine malnutrition hypothesis is that a signific

274 The minimization of the size of the NSCs leads to a large increase in capacitance, with a hi

275 d NSC extravasation in vitro, as compared to NSC encapsulated alone.

276 By applying this to NSC of the SVZ, we highlighted the importance of adult n

277 may be coordinated to communicate signals to NSCs.

278 and seasonal fluctuation of whole-tree total NSC pools as well as the contribution of individual orga

279 While whole-tree total NSC pools followed the conventional theory, sugar pools

280 We found that transformed NSCs are refractory to quiescence-inducing signals.

281 oody plants, we know little about whole-tree NSC storage.

282 s induce quiescence in surrounding wild-type NSCs in a cell-cell contact and Notch signaling-dependen

283 nteraction between transformed and wild-type NSCs isolated from the adult mouse subventricular zone n

284 at this subtype specification in NBs, unlike NSC differentiation, requires Polycomb-group-mediated re

285 Scaling up NSC concentrations to the ecosystem level, we find that

286 reby twigs had the highest and most variable NSC concentration, followed by branches and then trunk.

287 ter establishment by sonic hedgehog, ventral NSC identity became independent of this morphogen.

288 resulting in G(0) arrest, while more ventral NSCs undergo G(2) quiescence.

289 ibit higher activity in glioblastomas versus NSCs, are associated with poor clinical outcomes, and ar

290 In the absence of vimentin, NSCs have a reduced capacity to exit quiescence, a time

291 l of HD, using neural stem cells (ReNcell VM NSCs) stably transduced to express exon 1 huntingtin (HT

292 Microcephaly may result when NSC divisions are too slow, produce neurons too early or

293 ced capacity to exit quiescence, a time when NSCs are required to clear a wave of aggregated proteins

294 een implicated in opiate dependence, whether NSC neuronal differentiation and subsequent dendritogene

295 p; ortholog of p57(KIP2)) determines whether NSCs enter G(0) or G(2) quiescence during embryogenesis.

296 s in NSCs, where it colocalizes broadly with NSC regulator SOX2.

297 ithelium remodeling at the tissue level with NSC fate acquisition.

298 des of V-SVZ NSCs, and draw comparisons with NSCs in the SGZ.

299 spatial separation of the sub-ependymal zone NSC niche and the olfactory bulb, the region to which ne

300 down of Rab27a in dorsal subventricular zone NSCs and astrocytes increased the number of CD11b/IBA1 p