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Follicular atresia

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362:) is the loss of ovarian function before the age of 40 due to follicular dysfunction such as accelerated follicular atresia. POF may present itself with characteristics and symptoms such as loss of menstruation for at least 4 months and also increased serum follicle-stimulating hormone (FSH) concentration (greater than or equal to 40 IU/L). There may be many causes of POF, ranging from genetic disorders to surgery, radiation therapy, and exposure to environmental toxicants. Accelerated follicular atresia due to chromosomal and genomic defects accounts for up to one-half of all POF cases. For example, 259: 28: 392:
large (greater than 7 cm), cause abdominal pain, or rupture, in which case pain relievers or emergency surgery may be required. If the cyst lasts for longer than a few months, a physician may recommend surgical removal or testing to determine if it is cancerous. Ultrasound is a common method of visualizing a cyst to determine treatment.
438:. The mechanism of PCOS is unknown, but is multifactorial. It has been observed that certain genes related to steroid and androgenic hormone production may contribute to development of the disease in individuals, environmental factors such as insulin resistance and obesity, and passing down of genetics from first degree relatives. 242:
Anti-MΓΌllerian hormone (AMH) has been studied to be a key regulator in the ovaries in humans that inhibits follicular atresia. It has been proven that AMH reduces the growth of follicles and its upregulation proposes a potential pathophysiological pathway in PCOS. Using indirect comparators to derive
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age. Approximately 1% of mammalian follicles in ovaries undergo ovulation and the remaining 99% of follicles go through follicular atresia as they cycle through the growth phases. In summary, follicular atresia is a process that leads to the follicular loss and loss of oocytes, and any disturbance or
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cells. Oocytes are then able to mature within the follicle through meiosis. In humans with ovaries, this process occurs continuously, as they are born with a finite number of follicles (between 500,000-1,000,000 follicles), and about 99% of follicles undergo atresia. Only one follicle will be mature
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Diagnosis of PCOS is based on meeting two of the three clinical criteria based on the Rotterdam Criteria: chronic anovulation (the ovum is not released from the ovary during menstrual cycle), hyperandrogenism (increased levels of androgen hormones, such as testosterone), and large number of ovarian
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When an ovarian follicle fails to undergo atresia and release an egg, it can grow to form a cyst. This may be due to an overproduction of FSH or an inadequate supply of LH. Most follicular cysts are harmless and resolve on their own within several months. However, rarely a cyst will grow to be very
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Non-pharmacological management and treatment of PCOS include dietary intervention. While there is no one optimal diet or superior diet, as this disease is highly individualized, diets that impact weight loss and insulin resistance have been shown to improve reproductive function. Examples of these
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PCOS is correlated with other metabolic comorbidities. One of large concern is obesity and insulin resistance. This is of high interest when assessing treatment and management of PCOS. Other risk factors include traditional cardiovascular disease risk factors such as dyslipidemia and hypertension.
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Undergoing follicular atresia is necessary in order for mammals to maintain a healthy reproductive system. Mammalian ovaries ovulate about 1% of the follicles and the remaining follicles may go through atresia as it cycles through the growth phases. However, disorders in the regulation of follicle
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According to the gonadotropin theory, follicular depletion associated with incessant follicular atresia has also been hypothesized as a potential etiology for ovarian cancer, due to an increase in serum gonadotropins. This leads to an inflammatory environment which promotes cellular turnover and
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Pharmacological management may be recommended for those who have comorbid conditions, such as obesity, type 2 diabetes, etc. Guidelines suggest possible oral contraceptives in combination with metformin (anti-diabetic medication), and/or anti-androgen agents. As PCOS is a highly individualized
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to prepare the body for conception. If conception does not occur, then it will be shed and is known as the corpus albicans. It has been observed that this mechanism is important in regulating and maintaining a healthy reproductive system in mammals.
426:(i.e. loss of appetite, nausea, constipation, and unexpected weight loss). Many people who are diagnosed with ovarian cancer also report feeling very full fast and many of them having a feeling on unexpected continuous bloating in their abdomen. 403:
is highly prevalent amongst humans who have ovaries and leads to many deaths in the United States. Since FSH inhibits follicular atresia, the overproduction of FSH can lead to excessive follicle formation and increased risk of ovarian cancer.
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have been linked to follicular deficiencies. Smoking has also been found to increase follicular atresia and lead to premature ovarian failure. Some of the short term effects of POF are hot flashes, irregular heart beat/heart
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This type of follicular atresia is often considered the classic and most commonly observed form. In most species, it occurs throughout follicular development and is universally seen in large follicles (>5mm diameter).
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Naimi A, Movassaghpour AA, Hagh MF, Talebi M, Entezari A, Jadidi-Niaragh F, Solali S (February 2018). "TNF-related apoptosis-inducing ligand (TRAIL) as the potential therapeutic target in hematological malignancies".
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this hypothesis, exploring different patient populations such as individuals who have polycystic ovary syndrome (PCOS) help support the hypothesis that AMH may be a key regulator in inhibiting follicular atresia.
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The inability to regulate granulosa cell apoptosis and undergo follicular atresia, due to overexpression of certain genes, has been linked to the development of some hormone-related cancers (such as
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enough to release an egg and may be fertilized. Typically around 20 follicles mature each month but only a single follicle is ovulated; the follicle from which the oocyte was released becomes the
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Manabe N, Matsuda-Minehata F, Goto Y, Maeda A, Cheng Y, Nakagawa S, et al. (July 2008). "Role of cell death ligand and receptor system on regulation of follicular atresia in pig ovaries".
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diets include the DASH diet (Dietary Approach to Stop Hypertension) and the ketogenic diet. However it is important to consult a medical professional before starting on such diet is safe.
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Makarevich AV, FâldeőiovÑ M, Pivko J, KubovičovÑ E, Chrenek P (December 2018). "Histological characteristics of ovarian follicle atresia in dairy cows with different milk production".
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Follicular atresia occurs throughout all stages of follicular development, until the follicular reserve is completely exhausted. Exhaustion of the follicular reserve occurs at
140:(FSH), which promotes follicle development. Once the follicle has developed, it secretes estrogen, which in high levels decreases secretions of FSH. Granulosa cell 1797:
Zhang Z, Jia L, Feng Y, Zheng W (June 2009). "Overexpression of follicle-stimulating hormone receptor facilitates the development of ovarian epithelial cancer".
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This form of follicular atresia has only been observed in small follicles of dairy cows (< 5mm diameter), and has not been reported in any other species.
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is caused by follicular atresia. Breakdown of the follicles prevent them from releasing hormones such as estrogen. Progesterone levels also decrease during
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Lee K, Pisarska MD, Ko JJ, Kang Y, Yoon S, Ryou SM, et al. (October 2005). "Transcriptional factor FOXL2 interacts with DP103 and induces apoptosis".
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Yang R, Xu S, Zhao Z, Li J (February 2012). "Fas ligand expression and mediated activation of an apoptosis program in bovine follicular granulosa cells".
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system has been linked to abnormal follicle development, and increased numbers of secondary follicles as a result of the inability to induce apoptosis.
108:, which is typically around the age of 51 in humans with ovaries. The dramatic decrease in estrogen and progesterone levels that is characteristic of 434:
Polycystic Ovary Syndrome, or PCOS affects 6-12% of humans with ovaries of reproductive age in the United States, and is one of the common causes of
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is considered the underlying mechanism of follicular atresia, and has been associated with five ligand-receptor systems involved in cell death:
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cysts. Symptoms and characteristics of PCOS include irregular periods or missed periods, excess body hair or thinning hair, weight gain, acne.
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ensures that the follicle gets eliminated without triggering an inflammatory response. Antral follicular atresia causes no damage to basal
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Podfigurna-Stopa A, Czyzyk A, Grymowicz M, Smolarczyk R, Katulski K, Czajkowski K, Meczekalski B (September 2016).
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Asselin E, Xiao CW, Wang YF, Tsang BK (2000). "Mammalian follicular development and atresia: role of apoptosis".
498: 87:. The corpus luteum is the last stage of the ovarian follicles' lifecycle. It has an important role in secreting 423: 556:"Esculentoside A rescues granulosa cell apoptosis and folliculogenesis in mice with premature ovarian failure" 239:) and long form (cFLIPL), which are strongly expressed in granulosa cells, may act as anti-apoptotic factors. 418:
Ovarian cancer is characterized by some generalized symptoms such as bloating or swelling in the abdomen,
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in rats can prevent atresia of the ovarian follicle, while depressed levels have the opposite effect.
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have often been observed, penetrating the basal lamina during this type of follicular atresia. These
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protein, that is expressed on granulosa cells, mediates signals that induce apoptosis by binding
1186:"Tumor necrosis factor alpha inhibits ovulation and induces granulosa cell death in rat ovaries" 136:
process that depends dominantly on granulosa cell apoptosis. Follicular atresia is inhibited by
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and releasing an egg. It is a normal, naturally occurring progression that occurs as mammalian
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Teede HJ, Misso ML, Costello MF, Dokras A, Laven J, Moran L, et al. (September 2018).
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of the follicle can also be observed. Basal follicular atresia causes no damage to antral
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Yamamoto Y, Kuwahara A, Taniguchi Y, Yamasaki M, Tanaka Y, Mukai Y, et al. (2015).
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Histological view of an ovarian follicle. The egg is located within the smaller ring.
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Matsuda F, Inoue N, Goto Y, Maeda A, Cheng Y, Sakamaki K, Manabe N (October 2008).
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and therefore plays an important role in follicular atresia. Lack of a functional
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From studying dairy cows, two forms of follicular atresia have been identified:
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within the antral layers of the granulosa membrane and sometimes within the
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loss of functionality of this process can lead to many other conditions.
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condition, each individual's management and goals will look different.
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Basal follicular atresia is characterized by the destruction of
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because without any follicles, there is no development of the
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In addition, two intracellular inhibitor proteins, cellular
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Layers of a mature ovarian follicle right before ovulation.
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6, 7, 8, 9, and 10 to induce apoptosis in granulosa cells.
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breakdown and generation can lead to various pathologies:
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in the antral layers of the membrane can be observed.
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Oocytes 21: 2329: 2328: 2324: 2323: 2322: 2320: 2319: 2318: 2304: 2303: 2302: 2301: 2257: 2256: 2252: 2208: 2207: 2203: 2159: 2158: 2154: 2108: 2107: 2100: 2091: 2089: 2072: 2071: 2067: 2013: 2012: 2008: 1964: 1963: 1959: 1915: 1914: 1910: 1866: 1865: 1861: 1831: 1830: 1826: 1796: 1795: 1791: 1761: 1760: 1756: 1747: 1745: 1743: 1719:Cole L (2016). 1718: 1717: 1713: 1677: 1676: 1672: 1628: 1627: 1620: 1611: 1609: 1607: 1582: 1581: 1577: 1568: 1566: 1564: 1539: 1538: 1529: 1491: 1490: 1483: 1437: 1436: 1432: 1396: 1395: 1391: 1347: 1346: 1339: 1308: 1307: 1303: 1267: 1266: 1262: 1232: 1231: 1227: 1183: 1182: 1178: 1148: 1147: 1143: 1105: 1104: 1100: 1064: 1063: 1059: 1015: 1014: 1010: 974: 973: 966: 922: 921: 917: 887: 886: 882: 873: 871: 854: 853: 849: 795: 794: 790: 781: 779: 762: 761: 757: 713: 712: 708: 667:(10): e108343. 654: 653: 649: 605: 604: 597: 553: 552: 545: 538: 517: 516: 512: 507: 494:Ovarian reserve 460: 432: 398: 389: 368:Turner syndrome 356: 347: 316:granulosa cells 312: 295:pyknotic nuclei 287:granulosa cells 279: 256: 193:Fas antigen, a 126: 102: 76:granulosa cells 57: 23: 22: 15: 12: 11: 5: 2327: 2325: 2317: 2316: 2306: 2305: 2300: 2299: 2250: 2221:(6): 313–323. 2201: 2152: 2098: 2065: 2006: 1977:(1–2): 34–41. 1957: 1908: 1859: 1840:(3): 876–881. 1824: 1799:Cancer Letters 1789: 1754: 1741: 1711: 1690:(1–3): 51–54. 1670: 1641:(9): 983–990. 1618: 1605: 1575: 1562: 1527: 1500:(6): 510–516. 1481: 1430: 1389: 1360:(5): 337–341. 1337: 1301: 1280:(4): 561–566. 1260: 1241:(1): 148–154. 1225: 1196:(3): 107–115. 1176: 1141: 1098: 1077:(5): 314–320. 1057: 1028:(2): 145–151. 1008: 987:(5): 493–514. 964: 935:(2): 248–257. 915: 880: 847: 788: 755: 706: 647: 618:(4): 726–737. 595: 543: 536: 509: 508: 506: 503: 502: 501: 496: 491: 486: 481: 476: 471: 466: 459: 456: 431: 428: 401:Ovarian cancer 397: 396:Ovarian Cancer 394: 388: 385: 355: 352: 346: 343: 311: 308: 278: 275: 255: 252: 248:Nitrogen oxide 184: 183: 177: 171: 161: 155: 125: 122: 101: 98: 66:which secrete 56: 53: 24: 14: 13: 10: 9: 6: 4: 3: 2: 2326: 2315: 2312: 2311: 2309: 2295: 2291: 2286: 2281: 2277: 2273: 2269: 2265: 2261: 2254: 2251: 2246: 2242: 2238: 2234: 2229: 2224: 2220: 2216: 2212: 2205: 2202: 2197: 2193: 2189: 2185: 2180: 2175: 2171: 2167: 2163: 2156: 2153: 2148: 2144: 2139: 2134: 2129: 2124: 2120: 2116: 2112: 2105: 2103: 2099: 2088: 2084: 2080: 2076: 2069: 2066: 2061: 2057: 2053: 2049: 2044: 2039: 2034: 2029: 2025: 2021: 2017: 2010: 2007: 2002: 1998: 1993: 1988: 1984: 1980: 1976: 1972: 1968: 1961: 1958: 1953: 1949: 1944: 1939: 1935: 1931: 1927: 1923: 1919: 1912: 1909: 1904: 1900: 1896: 1892: 1887: 1882: 1878: 1874: 1870: 1863: 1860: 1855: 1851: 1847: 1843: 1839: 1835: 1828: 1825: 1820: 1816: 1812: 1808: 1804: 1800: 1793: 1790: 1785: 1781: 1777: 1773: 1769: 1765: 1758: 1755: 1744: 1738: 1734: 1730: 1726: 1722: 1715: 1712: 1707: 1703: 1698: 1693: 1689: 1685: 1681: 1674: 1671: 1666: 1662: 1657: 1652: 1648: 1644: 1640: 1636: 1632: 1625: 1623: 1619: 1608: 1602: 1598: 1594: 1590: 1586: 1579: 1576: 1565: 1559: 1555: 1554:10.5772/32465 1551: 1547: 1543: 1536: 1534: 1532: 1528: 1523: 1519: 1515: 1511: 1507: 1503: 1499: 1495: 1488: 1486: 1482: 1477: 1473: 1468: 1463: 1458: 1453: 1449: 1445: 1441: 1434: 1431: 1426: 1422: 1417: 1412: 1408: 1404: 1400: 1393: 1390: 1385: 1381: 1376: 1371: 1367: 1363: 1359: 1355: 1351: 1344: 1342: 1338: 1333: 1329: 1325: 1321: 1317: 1313: 1305: 1302: 1297: 1293: 1288: 1283: 1279: 1275: 1271: 1264: 1261: 1256: 1252: 1248: 1244: 1240: 1236: 1229: 1226: 1221: 1217: 1212: 1207: 1203: 1199: 1195: 1191: 1187: 1180: 1177: 1172: 1168: 1164: 1160: 1156: 1152: 1145: 1142: 1137: 1133: 1129: 1125: 1121: 1117: 1113: 1109: 1102: 1099: 1094: 1090: 1085: 1080: 1076: 1072: 1068: 1061: 1058: 1053: 1049: 1045: 1041: 1036: 1031: 1027: 1023: 1019: 1012: 1009: 1004: 1000: 995: 990: 986: 982: 978: 971: 969: 965: 960: 956: 951: 946: 942: 938: 934: 930: 926: 919: 916: 911: 907: 903: 899: 895: 891: 884: 881: 870: 866: 862: 858: 851: 848: 843: 839: 834: 829: 824: 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InTech. 1450:: 752410. 874:2022-08-04 861:StatPearls 782:2022-07-26 769:StatPearls 505:References 329:the basal 254:Morphology 203:Fas ligand 199:Fas ligand 130:hormonally 55:Background 2245:238411748 2196:227078090 479:Oogenesis 299:Apoptosis 283:apoptosis 218:caspase 3 168:apoptosis 166:-related 153:receptors 142:apoptosis 134:apoptotic 124:Mechanism 114:menopause 110:menopause 106:menopause 100:Menopause 44:ovulating 2308:Category 2294:30052961 2237:34610596 2188:33211867 2147:35924049 2087:29083730 2060:21331891 2052:21299513 2001:30859785 1952:19012860 1903:21975528 1895:21119601 1873:Oncogene 1854:16153597 1819:19181441 1784:22343225 1706:26374525 1665:27091671 1522:51697201 1514:30022512 1476:34867795 1425:27174394 1384:33041549 1332:29288972 1296:11277875 1255:22155318 1220:26161038 1171:18638134 1136:30459318 1128:10810203 1093:18603835 1052:10644197 1044:16010689 1003:15514456 869:30969526 842:24788203 802:PLOS ONE 777:31424854 750:13689486 742:29743261 701:25310678 661:PLOS ONE 642:30906205 590:32759462 458:See also 222:caspases 89:estrogen 68:hormones 40:follicle 2285:6112576 2138:9340349 1992:7325817 1943:2713057 1656:4987394 1467:8640491 1375:7515982 1211:4490172 959:6401767 910:9074768 833:4008600 810:Bibcode 692:4195570 669:Bibcode 633:6429023 581:7521512 233:protein 60:Ovaries 48:ovaries 2292:  2282:  2243:  2235:  2194:  2186:  2145:  2135:  2085:  2058:  2050:  1999:  1989:  1950:  1940:  1901:  1893:  1852:  1817:  1782:  1739:  1704:  1663:  1653:  1603:  1560:  1520:  1512:  1474:  1464:  1423:  1382:  1372:  1330:  1294:  1253:  1218:  1208:  1169:  1134:  1126:  1091:  1050:  1042:  1001:  957:  950:436863 947:  908:  867:  840:  830:  775:  748:  740:  699:  689:  640:  630:  588:  578:  534:  291:antrum 277:Antral 272:basal. 268:antral 237:cFLIPS 2241:S2CID 2192:S2CID 2056:S2CID 1899:S2CID 1518:S2CID 1132:S2CID 1048:S2CID 746:S2CID 560:Aging 310:Basal 229:FLICE 214:TRAIL 180:PFG-5 174:APO-3 80:theca 2290:PMID 2233:PMID 2184:PMID 2143:PMID 2083:PMID 2048:PMID 1997:PMID 1948:PMID 1891:PMID 1850:PMID 1815:PMID 1780:PMID 1737:ISBN 1702:PMID 1661:PMID 1601:ISBN 1558:ISBN 1510:PMID 1472:PMID 1421:PMID 1380:PMID 1328:PMID 1292:PMID 1251:PMID 1235:Gene 1216:PMID 1167:PMID 1124:PMID 1089:PMID 1040:PMID 999:PMID 955:PMID 906:PMID 865:PMID 838:PMID 773:PMID 738:PMID 697:PMID 638:PMID 586:PMID 532:ISBN 270:and 91:and 70:and 2280:PMC 2272:doi 2223:doi 2174:doi 2170:106 2133:PMC 2123:doi 2038:hdl 2028:doi 1987:PMC 1979:doi 1938:PMC 1930:doi 1881:doi 1842:doi 1838:336 1807:doi 1803:278 1772:doi 1729:doi 1692:doi 1651:PMC 1643:doi 1593:doi 1550:doi 1502:doi 1462:PMC 1452:doi 1411:doi 1370:PMC 1362:doi 1320:doi 1282:doi 1278:121 1243:doi 1239:493 1206:PMC 1198:doi 1159:doi 1116:doi 1079:doi 1030:doi 989:doi 945:PMC 937:doi 898:doi 828:PMC 818:doi 728:doi 724:156 687:PMC 677:doi 628:PMC 620:doi 576:PMC 568:doi 524:doi 285:of 164:TNF 158:Fas 2310:: 2288:. 2278:. 2268:33 2266:. 2262:. 2239:. 2231:. 2219:77 2217:. 2213:. 2190:. 2182:. 2168:. 2164:. 2141:. 2131:. 2119:13 2117:. 2113:. 2101:^ 2077:. 2054:. 2046:. 2036:. 2024:51 2022:. 2018:. 1995:. 1985:. 1973:. 1969:. 1946:. 1936:. 1924:. 1920:. 1897:. 1889:. 1877:30 1875:. 1871:. 1848:. 1836:. 1813:. 1801:. 1778:. 1768:55 1766:. 1735:. 1700:. 1688:59 1686:. 1682:. 1659:. 1649:. 1639:39 1637:. 1633:. 1621:^ 1599:. 1556:. 1530:^ 1516:. 1508:. 1498:47 1496:. 1484:^ 1470:. 1460:. 1448:12 1446:. 1442:. 1419:. 1407:33 1405:. 1401:. 1378:. 1368:. 1358:70 1356:. 1352:. 1340:^ 1326:. 1316:98 1314:. 1290:. 1276:. 1272:. 1249:. 1237:. 1214:. 1204:. 1194:14 1192:. 1188:. 1165:. 1155:43 1153:. 1130:. 1122:. 1110:. 1087:. 1075:54 1073:. 1069:. 1046:. 1038:. 1026:72 1024:. 1020:. 997:. 985:50 983:. 979:. 967:^ 953:. 943:. 933:71 931:. 927:. 904:. 894:59 892:. 859:. 836:. 826:. 816:. 804:. 800:. 767:. 744:. 736:. 722:. 718:. 695:. 685:. 675:. 663:. 659:. 636:. 626:. 616:15 614:. 610:. 598:^ 584:. 574:. 564:12 562:. 558:. 546:^ 530:. 422:, 366:, 205:/ 2296:. 2274:: 2247:. 2225:: 2198:. 2176:: 2149:. 2125:: 2095:. 2062:. 2040:: 2030:: 2003:. 1981:: 1975:8 1954:. 1932:: 1926:9 1905:. 1883:: 1856:. 1844:: 1821:. 1809:: 1786:. 1774:: 1751:. 1731:: 1708:. 1694:: 1667:. 1645:: 1615:. 1595:: 1572:. 1552:: 1524:. 1504:: 1478:. 1454:: 1427:. 1413:: 1386:. 1364:: 1334:. 1322:: 1298:. 1284:: 1257:. 1245:: 1222:. 1200:: 1173:. 1161:: 1138:. 1118:: 1112:9 1095:. 1081:: 1054:. 1032:: 1005:. 991:: 961:. 939:: 912:. 900:: 877:. 844:. 820:: 812:: 806:9 785:. 752:. 730:: 703:. 679:: 671:: 665:9 644:. 622:: 592:. 570:: 540:. 526:: 20:)

Index

Ovarian follicle atresia

follicle
ovulating
ovaries
Ovaries
ovarian follicles
hormones
oocytes. Oocytes
granulosa cells
theca
corpus luteum
estrogen
progesterone
menopause
menopause
menopause
corpus luteum
hormonally
apoptotic
follicle-stimulating hormone
apoptosis
tumor necrosis factor alpha
receptors
Fas
TNF
apoptosis
APO-3
PFG-5
tumor necrosis factor-alpha

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