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1 ngle layer of somatic (granulosa) cells in a primordial follicle.
2 , but was low in oocytes within newly formed primordial follicles.
3 oximately 33% of the oocytes survive to form primordial follicles.
4 ed in dramatically smaller ovaries and fewer primordial follicles.
5 ion characterized by premature exhaustion of primordial follicles.
6 st in non-growing oocytes (NGOs) residing in primordial follicles.
7 nce of meiotic arrest in oocytes residing in primordial follicles.
8 i, was ablated in mouse oocytes beginning in primordial follicles.
9 ollicle and activates an excessive number of primordial follicles.
10 ia that support the growth and maturation of primordial follicles.
11 alian females, germ cells remain arrested as primordial follicles.
12 ontrol cell death pathways in the oocytes of primordial follicles.
13 BMP2-BMPR system leading to the formation of primordial follicles.
14 cysts into individual oocytes housed within primordial follicles.
15 mature activation of all dormant oocytes and primordial follicles.
16 spermatogonial stem cells and the origin of primordial follicles.
17 erage that eventually give rise to about six primordial follicles.
18 serum estradiol levels and the formation of primordial follicles.
19 nation of oocyte numbers and the assembly of primordial follicles.
20 ferentiate into granulosa cells of quiescent primordial follicles.
21 m cells; (c) pre-granulosa cells surrounding primordial follicles.
22 the survival of germ cells in newly formed (primordial) follicles.
23 sts may ensure that oocytes destined to form primordial follicles acquire populations of functional m
25 y, homozygous Kit(Y719F) female mice undergo primordial follicle activation and are fertile, demonstr
26 sis of the contribution of Kit in regulating primordial follicle activation and early follicle growth
27 ib, and ruxolitinib can specifically inhibit primordial follicle activation and repress folliculogene
28 n with the unique characteristic of blocking primordial follicle activation that could be exploited t
29 3-kinase (PI3K) signalling pathway controls primordial follicle activation through the forkhead tran
32 and Foxo3 nuclear export, thereby triggering primordial follicle activation, defining the steps by wh
37 norepinephrine fails to maintain a quiescent primordial follicle and activates an excessive number of
38 the somatic pfGCs initiate the activation of primordial follicles and govern the quiescence or awaken
39 ryonic exposure to ATZ reduces the number of primordial follicles and increases the incidence of mult
40 ctive-caspase-3 (p = 0.0001) staining in the primordial follicles and no change in the growing follic
41 bout how the pfGCs control the activation of primordial follicles and the developmental fates of dorm
42 ads and performed lineage tracing to analyze primordial follicles and wave 1 medullar follicles durin
43 ncreased offspring, accelerated depletion of primordial follicles, and ultimately premature infertili
47 resenting two mechanisms: an initial pool of primordial follicles as the only follicle source (fixed
49 erm cell cyst (GCC) breakdown; (iv) advanced primordial follicle assembly and primary follicle transi
52 Foxo3 is imported into the nucleus during primordial follicle assembly, and is exported upon activ
54 eport that some quiescent primary oocytes in primordial follicles become senescent in adult mouse ova
55 mouse neonatal germline cysts and oocytes of primordial follicles but disperses as follicles begin to
56 specifically causes apoptotic cell death of primordial follicles but does not affect other periphera
57 tro, increased the number of postnatal mouse primordial follicles by 30% when administered to neonata
58 ary are dormant oocytes that are enclosed in primordial follicles by several somatic cells, which we
61 C57/Bl6 mouse ovaries densely populated with primordial follicles, CCND2 protein co-localised and was
65 OR inhibition preserves the ovarian reserve, primordial follicle counts, serum anti-Mullerian hormone
69 in Kit(Y719F) ovaries, including accelerated primordial follicle depletion and accumulation of morpho
70 varian insufficiency is chemotherapy-induced primordial follicle depletion, which has been proposed t
71 pre-granulosa cells in time and space, with primordial follicles deriving from later emerging pre-gr
73 to granulosa cells after the newly assembled primordial follicles develop into growing primary follic
74 ation to immune-deficient mice for 6 months, primordial follicles developed to the preovulatory stage
75 and ANM are shown to correspond to gaps when primordial follicles fail to grow for 7 and 12 days, res
76 riments suggest that NR5A2 expression poises primordial follicles for entry into the developing pool.
77 gnaling and KIT ligand in granulosa cells of primordial follicles for follicle activation and for rep
80 ole in perinatal germline cyst breakdown and primordial follicle formation by regulating E-cadherin j
81 rks that regulate oocyte differentiation and primordial follicle formation during early, postnatal mo
82 significantly suppressed cyst breakdown and primordial follicle formation in cultured mouse ovaries.
84 rane-impermeable BSA-conjugated P4 inhibited primordial follicle formation similar to that by P4.
87 nerate a list of candidate genes involved in primordial follicle formation, including podocalyxin (Po
88 ment with an FSH-antiserum, which suppressed primordial follicle formation, prevented the decline in
89 signaling plays a role in cyst breakdown and primordial follicle formation, we used ovary organ cultu
98 model illustrates the decline in the pool of primordial follicles from age 20 to menopause as reporte
103 eficiency prevents elimination of oocytes in primordial follicles in female mice exposed to radiation
104 st ensure that the reserve of oocytes within primordial follicles in humans lasts for up to 50 years,
108 ovary results in the formation of many fewer primordial follicles in the juvenile ovary, although the
109 fetal development and consists of quiescent primordial follicles in the ovarian cortex each composed
110 and theca cell recruitment as well as fewer primordial follicles in the ovarian cortex, causing a fa
111 an reserve represents the stock of quiescent primordial follicles in the ovary which is gradually dep
112 lt female Bax-/- mice possess threefold more primordial follicles in their ovarian reserve than their
117 e diepoxide (VCD), selective for primary and primordial follicles, is injected intraperitonelly in an
118 the Foxl2 lineage tag also marked about 400 primordial follicles, located near the medullary-cortica
119 ocyte-specific Trp63 knockout mice prevented primordial follicle loss and maintained reproductive fun
120 es and that senescent cell clearance reduced primordial follicle loss and mitigated ovarian aging phe
122 , pubertal abnormalities in females, ovarian primordial follicle loss and polycystic ovary disease we
123 re, we have probed how stochastic control of primordial follicle loss might relate to the distributio
124 essential functional unit of the ovary, the primordial follicle, occurs during fetal life in humans.
125 RNA-sequencing on laser-captured individual primordial follicle oocytes 12 h after a single cyclopho
127 qRT-PCR and immunostaining confirmed that in primordial follicle oocytes, cyclophosphamide did not ch
129 number and an increase in the proportion of primordial follicles (PMFs), with smaller oocytes within
132 disease (PCO) and a decrease in the ovarian primordial follicle pool size resembling primary ovarian
133 cle source (fixed pool model), or an initial primordial follicle pool supplemented by germline stem c
134 ility with major defects in stability of the primordial follicle pool, ovarian folliculogenesis, ovul
139 cific roles of Kit in the maintenance of the primordial follicle reserve and in the primary to second
141 germ-cell toxicant busulphan eliminates the primordial follicle reserve by early adulthood without i
142 cell cyst breakdown and establishment of the primordial follicle reserve during a critical window of
145 and primordial follicles were positive, with primordial follicles showing only weak focal positivity.
146 y inactivated the mouse Smc1beta gene at the primordial follicle stage shortly after birth, when oocy
147 be expressed during prophase I prior to the primordial follicle stage to ensure SCC up to advanced a
148 h 2 mg/kg cisplatin for 15 days can activate primordial follicles, suggesting that the response in th
149 H) induced a greater proportion of quiescent primordial follicles than control ExECs, indicating supp
150 lish associations with somatic cells to form primordial follicles that create a store of germ cells (
151 The ovary contains oocytes within immature (primordial) follicles that are fixed in number at birth.
152 secondary follicles were transferred back to primordial follicles, the earliest stage of follicular d
153 nalling in the maintenance and activation of primordial follicles, through SMAD-dependent and indepen
154 us AMH show that the transfer of non-growing primordial follicles to the active state can be slowed e
156 an ovaries, immature oocytes are reserved in primordial follicles until their activation for potentia
157 ing an individual woman's ovarian reserve of primordial follicles using mathematical random walks rep
158 ggesting that the response in the oocytes of primordial follicles was dependent on cisplatin concentr
160 ugh embryonic gonadogenesis appeared normal, primordial follicles were not formed at birth, and massi
163 survival is dependent upon the formation of primordial follicles, which occurs during fetal life in
164 oocytes are packaged into compact structures-primordial follicles-which remain inert for prolonged in
165 f 5 mg/kg cisplatin: the death of oocytes in primordial follicles without indication of activation.