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1 ngle layer of somatic (granulosa) cells in a primordial follicle.
2 oximately 33% of the oocytes survive to form primordial follicles.
3 BMP2-BMPR system leading to the formation of primordial follicles.
4 cysts into individual oocytes housed within primordial follicles.
5 mature activation of all dormant oocytes and primordial follicles.
6 spermatogonial stem cells and the origin of primordial follicles.
7 erage that eventually give rise to about six primordial follicles.
8 alian females, germ cells remain arrested as primordial follicles.
9 serum estradiol levels and the formation of primordial follicles.
10 nation of oocyte numbers and the assembly of primordial follicles.
11 m cells; (c) pre-granulosa cells surrounding primordial follicles.
12 , but was low in oocytes within newly formed primordial follicles.
13 the survival of germ cells in newly formed (primordial) follicles.
14 sts may ensure that oocytes destined to form primordial follicles acquire populations of functional m
15 y, homozygous Kit(Y719F) female mice undergo primordial follicle activation and are fertile, demonstr
16 sis of the contribution of Kit in regulating primordial follicle activation and early follicle growth
17 n with the unique characteristic of blocking primordial follicle activation that could be exploited t
18 3-kinase (PI3K) signalling pathway controls primordial follicle activation through the forkhead tran
21 and Foxo3 nuclear export, thereby triggering primordial follicle activation, defining the steps by wh
26 the somatic pfGCs initiate the activation of primordial follicles and govern the quiescence or awaken
27 ryonic exposure to ATZ reduces the number of primordial follicles and increases the incidence of mult
28 bout how the pfGCs control the activation of primordial follicles and the developmental fates of dorm
29 ncreased offspring, accelerated depletion of primordial follicles, and ultimately premature infertili
33 resenting two mechanisms: an initial pool of primordial follicles as the only follicle source (fixed
34 erm cell cyst (GCC) breakdown; (iv) advanced primordial follicle assembly and primary follicle transi
35 Foxo3 is imported into the nucleus during primordial follicle assembly, and is exported upon activ
37 mouse neonatal germline cysts and oocytes of primordial follicles but disperses as follicles begin to
38 specifically causes apoptotic cell death of primordial follicles but does not affect other periphera
39 tro, increased the number of postnatal mouse primordial follicles by 30% when administered to neonata
40 ary are dormant oocytes that are enclosed in primordial follicles by several somatic cells, which we
44 OR inhibition preserves the ovarian reserve, primordial follicle counts, serum anti-Mullerian hormone
48 in Kit(Y719F) ovaries, including accelerated primordial follicle depletion and accumulation of morpho
49 varian insufficiency is chemotherapy-induced primordial follicle depletion, which has been proposed t
51 to granulosa cells after the newly assembled primordial follicles develop into growing primary follic
52 ation to immune-deficient mice for 6 months, primordial follicles developed to the preovulatory stage
53 gnaling and KIT ligand in granulosa cells of primordial follicles for follicle activation and for rep
55 ole in perinatal germline cyst breakdown and primordial follicle formation by regulating E-cadherin j
56 significantly suppressed cyst breakdown and primordial follicle formation in cultured mouse ovaries.
58 rane-impermeable BSA-conjugated P4 inhibited primordial follicle formation similar to that by P4.
60 nerate a list of candidate genes involved in primordial follicle formation, including podocalyxin (Po
61 ment with an FSH-antiserum, which suppressed primordial follicle formation, prevented the decline in
62 signaling plays a role in cyst breakdown and primordial follicle formation, we used ovary organ cultu
71 model illustrates the decline in the pool of primordial follicles from age 20 to menopause as reporte
76 ovary results in the formation of many fewer primordial follicles in the juvenile ovary, although the
77 and theca cell recruitment as well as fewer primordial follicles in the ovarian cortex, causing a fa
78 an reserve represents the stock of quiescent primordial follicles in the ovary which is gradually dep
79 lt female Bax-/- mice possess threefold more primordial follicles in their ovarian reserve than their
81 e diepoxide (VCD), selective for primary and primordial follicles, is injected intraperitonelly in an
83 , pubertal abnormalities in females, ovarian primordial follicle loss and polycystic ovary disease we
84 essential functional unit of the ovary, the primordial follicle, occurs during fetal life in humans.
88 disease (PCO) and a decrease in the ovarian primordial follicle pool size resembling primary ovarian
89 cle source (fixed pool model), or an initial primordial follicle pool supplemented by germline stem c
93 cific roles of Kit in the maintenance of the primordial follicle reserve and in the primary to second
95 germ-cell toxicant busulphan eliminates the primordial follicle reserve by early adulthood without i
96 cell cyst breakdown and establishment of the primordial follicle reserve during a critical window of
98 and primordial follicles were positive, with primordial follicles showing only weak focal positivity.
99 y inactivated the mouse Smc1beta gene at the primordial follicle stage shortly after birth, when oocy
100 be expressed during prophase I prior to the primordial follicle stage to ensure SCC up to advanced a
101 H) induced a greater proportion of quiescent primordial follicles than control ExECs, indicating supp
102 The ovary contains oocytes within immature (primordial) follicles that are fixed in number at birth.
103 secondary follicles were transferred back to primordial follicles, the earliest stage of follicular d
104 us AMH show that the transfer of non-growing primordial follicles to the active state can be slowed e
106 ugh embryonic gonadogenesis appeared normal, primordial follicles were not formed at birth, and massi
108 survival is dependent upon the formation of primordial follicles, which occurs during fetal life in
109 oocytes are packaged into compact structures-primordial follicles-which remain inert for prolonged in
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