• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

不育患者人类精子头部缺失:一种与受精受损相关的综合征。

Lack of a head in human spermatozoa from sterile patients: a syndrome associated with impaired fertilization.

作者信息

Chemes H E, Carizza C, Scarinci F, Brugo S, Neuspiller N, Schwarsztein L

出版信息

Fertil Steril. 1987 Feb;47(2):310-6. doi: 10.1016/s0015-0282(16)50011-9.

DOI:10.1016/s0015-0282(16)50011-9
PMID:3545911
Abstract

Three patients with primary sterility in whom the majority of spermatozoa lacked a normally implanted head are presented. A small cephalic knob was evident in most of them by routine colorimetric techniques, and the Feulgen reaction failed to show any deoxyribose nucleic acid. The morphologic features of the tails was normal. Few loose sperm heads were observed in the ejaculates. Even though motility was decreased, there were numerous acephalic sperms with different degrees of forward motility. Electron microscopy showed a well-organized structure of the centrioles and connecting piece, which were located in the neck region within a small cytoplasmic mass, but no chromatin was detected in any case. Studies on immature spermatids present in semen evidenced an independent anomalous development of heads and tails and suggested that they became separated at the end of spermatid maturation. This anomaly, of probable genetic origin, is interpreted to be due either to an alteration in the mechanism of migration and positioning of the tail on the caudal pole of the nucleus or to an interference with the formation of the implantation fossa of the head, which normally accommodates the connecting piece.

摘要

本文报告了3例原发性不育患者,其大多数精子头部植入异常。通过常规比色技术,在大多数患者中可见一个小的头部小结,福尔根反应未显示任何脱氧核糖核酸。尾部的形态特征正常。在射精物中观察到少量游离的精子头部。尽管活力下降,但仍有许多无头精子具有不同程度的向前运动能力。电子显微镜显示中心粒和连接段结构良好,位于颈部区域的一小团细胞质内,但在任何情况下均未检测到染色质。对精液中未成熟精子细胞的研究表明,头部和尾部存在独立的异常发育,并提示它们在精子细胞成熟末期分离。这种异常可能源于遗传,被解释为要么是尾部在细胞核尾极的迁移和定位机制发生改变,要么是头部植入窝的形成受到干扰,而植入窝通常容纳连接段。

相似文献

1
Lack of a head in human spermatozoa from sterile patients: a syndrome associated with impaired fertilization.不育患者人类精子头部缺失:一种与受精受损相关的综合征。
Fertil Steril. 1987 Feb;47(2):310-6. doi: 10.1016/s0015-0282(16)50011-9.
2
Ultrastructural study of the decapitated sperm defect in an infertile man.一名不育男性断头精子缺陷的超微结构研究。
J Reprod Fertil. 1981 Nov;63(2):543-9. doi: 10.1530/jrf.0.0630543.
3
Acephalic spermatozoa and abnormal development of the head-neck attachment: a human syndrome of genetic origin.
Hum Reprod. 1999 Jul;14(7):1811-8. doi: 10.1093/humrep/14.7.1811.
4
Decapitated and decaudated spermatozoa in man, and pathogenesis based on the ultrastructure.人类中的无头和无尾精子及其基于超微结构的发病机制。
Int J Androl. 2000 Apr;23(2):109-15. doi: 10.1046/j.1365-2605.2000.t01-1-00217.x.
5
Morphogenesis of 'decapitated' spermatozoa in a man.一名男性中“断头”精子的形态发生。
J Reprod Fertil. 1984 Mar;70(2):395-7. doi: 10.1530/jrf.0.0700395.
6
Sperm with fibrous sheath dysplasia and anomalies in head-neck junction: focus on centriole and centrin 1.伴有纤维鞘发育异常及头颈连接处异常的精子:聚焦于中心粒和中心蛋白1
Andrologia. 2017 Sep;49(7). doi: 10.1111/and.12701. Epub 2016 Sep 5.
7
TMF/ARA160: A key regulator of sperm development.TMF/ARA160:精子发育的关键调节因子。
Dev Biol. 2010 Dec 1;348(1):12-21. doi: 10.1016/j.ydbio.2010.07.033. Epub 2010 Aug 5.
8
Morphogenesis of the decapitated and decaudated sperm defect in two brothers.两兄弟中无头无尾精子缺陷的形态发生
Gamete Res. 1989 Jun;23(2):181-8. doi: 10.1002/mrd.1120230205.
9
Origin, development and ultrastructure of boar spermatozoa with folded tails and with two tails.具有折叠尾和双尾的公猪精子的起源、发育及超微结构
Hum Reprod. 1992 Apr;7(4):523-8. doi: 10.1093/oxfordjournals.humrep.a137683.
10
Development of the Connecting Piece in ODF1-Deficient Mouse Spermatids.ODF1 缺陷型小鼠精母细胞连接段的发育。
Int J Mol Sci. 2022 Sep 7;23(18):10280. doi: 10.3390/ijms231810280.

引用本文的文献

1
A systematic review and evidence assessment of monogenic gene-disease relationships in human male infertility.人类男性不育中单基因基因-疾病关系的系统评价与证据评估
Front Endocrinol (Lausanne). 2025 Aug 28;16:1643543. doi: 10.3389/fendo.2025.1643543. eCollection 2025.
2
Pathogenesis of acephalic spermatozoa syndrome caused by PMFBP1 mutation.由PMFBP1突变引起的无头精子症综合征的发病机制。
Basic Clin Androl. 2024 Dec 13;34(1):22. doi: 10.1186/s12610-024-00240-3.
3
Loss of CCDC188 causes male infertility with defects in the sperm head-neck connection in mice†.
CCDC188缺失导致小鼠雄性不育,并伴有精子头部与颈部连接缺陷† 。
Biol Reprod. 2025 Jan 14;112(1):169-178. doi: 10.1093/biolre/ioae137.
4
The proximal centriole-like structure maintains nucleus-centriole architecture in sperm.近端中心粒样结构维持精子中的核-中心体结构。
J Cell Sci. 2024 Sep 1;137(17). doi: 10.1242/jcs.262311. Epub 2024 Sep 6.
5
A novel homozygous TSGA10 missense variant causes acephalic spermatozoa syndrome in a Pakistani family.一种新的纯合子TSGA10错义变异导致一个巴基斯坦家庭出现无头精子症综合征。
Basic Clin Androl. 2024 Feb 5;34(1):4. doi: 10.1186/s12610-024-00220-7.
6
Semen parameters are seriously affected in acephalic spermatozoa syndrome.在无头精子症综合征中,精液参数受到严重影响。
Basic Clin Androl. 2022 Aug 26;32(1):20. doi: 10.1186/s12610-022-00170-y.
7
BmPMFBP1 regulates the development of eupyrene sperm in the silkworm, Bombyx mori.BmPMFBP1 调控家蚕有精蛹的精子发生。
PLoS Genet. 2022 Mar 21;18(3):e1010131. doi: 10.1371/journal.pgen.1010131. eCollection 2022 Mar.
8
Genetic pathogenesis of acephalic spermatozoa syndrome: past, present, and future.无头精子症综合征的遗传发病机制:过去、现在和未来。
Asian J Androl. 2022 May-Jun;24(3):231-237. doi: 10.4103/aja202198.
9
The Transformation of the Centrosome into the Basal Body: Similarities and Dissimilarities between Somatic and Male Germ Cells and Their Relevance for Male Fertility.中心体向基体的转化:体细胞和雄性生殖细胞之间的相似性和差异性及其与男性生育力的关系。
Cells. 2021 Aug 31;10(9):2266. doi: 10.3390/cells10092266.
10
Pathogenic Variants in Cause Acephalic Spermatozoa Syndrome.导致无头精子症综合征的致病变异。
Front Cell Dev Biol. 2021 Aug 6;9:676246. doi: 10.3389/fcell.2021.676246. eCollection 2021.