Quantitative Investigations on Human Testicular Biopsies

Roosen‐Runge, Edward C.; Marberger, E; Nelson, Warren O.

doi:10.1016/s0015-0282(16)61353-5

Cited by 25 publications

(17 citation statements)

References 5 publications

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“…The reduced SMAD3-positive pachytene spermatocyte numbers in patients with Hyp or MA (Hentrich et al 2011) was also described without marker expression analysis in cases with reduced sperm cell numbers (Roosen-Runge et al 1957, Zukerman et al 1978. In contrast to the retained SMAD3 protein expression in cases with impaired spermatogenesis, the BOULE protein (expressed in human leptotene to pachytene spermatocytes in Nsp) was completely absent in cases with MA (Luetjens et al 2004).…”

Section: Discussionmentioning

confidence: 94%

Role of compensatory meiosis mechanisms in human spermatogenesis

Borgers¹,

Wolter²,

Hentrich³

et al. 2014

Reproduction

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Disturbances of checkpoints in distinct stages of spermatogenesis (mitosis, meiosis, and spermiogenesis) contribute to impaired spermatogenesis; however, the efficiency of meiotic entry has not been investigated in more detail. In this study, we analyzed azoospermic patients with defined spermatogenic defects by the use of octamer-binding protein 2 for type A spermatogonia, sarcoma antigen 1 for mitosis-meiosis transition and SMAD3 for pachytene spermatocytes. Especially patients with maturation arrest (MA) at the level of primary spermatocytes showed significantly reduced numbers of spermatogonia compared with patients with histologically intact spermatogenesis or patients with hypospermatogenesis (Hyp). For a detailed individual classification of the patients, we distinguished between 'high efficiency of meiotic entry' (high numbers of pachytene spermatocytes) and 'low efficiency of meiotic entry' (low numbers of pachytene spermatocytes). Only patients with histologically normal spermatogenesis (Nsp) and patients with Hyp showed normal numbers of spermatogonia and a high efficiency of meiotic entry. Of note, only patients with histologically Nsp or patients with Hyp could compensate low numbers of spermatogonia with a high efficiency of meiotic entry. In contrast, patients with MA always showed a low efficiency of meiotic entry. This is the first report on patients with impaired spermatogenesis, showing that half of the patients with Hyp but all patients with MA cannot compensate reduced numbers in spermatogonia with a highly efficient meiosis. Thus, we suggest that compensatory meiosis mechanisms in human spermatogenesis exist.

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Section: Discussionmentioning

confidence: 94%

Role of compensatory meiosis mechanisms in human spermatogenesis

Borgers¹,

Wolter²,

Hentrich³

et al. 2014

Reproduction

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“…One criticism of this study is that testicular biopsy samples were not always fully rcpresentative, since at least 100 cross sectionr of seminiferous tubules should be microscopically examined before the sampling can be regarded as adequate (Rosen-Runge, 1956). In 45Vo of cases the biopsies contained sufficient tubules but, more importantly, adequate biopsies were obtained in the 3 cases with high pre-biopsy titres; nevertheless, there were no foci of lymphocytic, tions of autoimmunity such as delayed hypersensitivity.…”

Section: Discussionmentioning

confidence: 96%

Studies of Testicular and Epididymal Damage in Relation to the Occurrence of Antisperm Antibodies

Hargreave

Busuttil

Elton

et al. 1982

British Journal of Urology

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The relationship between testicular histopathology, follicle stimulating hormone levels, sperm density and the presence of antisperm antibodies was investigated. There was no association between damage to the seminiferous tubules and the presence of agglutinating or immobilising antisperm antibodies. In 2 patients with congenital obstructive azoospermia and pre-biopsy circulating antisperm antibody there was extensive lymphocytic, macrophage and plasma cell infiltration, fibrosis and perivasculitis on epididymal biopsy. Breaches in the blood epididymis barrier are worthy of further investigation when considering the genesis of antisperm antibodies.

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“…The above interpretations of spermatogonial proliferation in humans are different from that of Roosen-Runge (1952, 1956 or Roosen-Runge and Barlow (1953). On the basis of nuclear size or length of the metaphase plate, they concluded that spermatogonia underwent 7 divisions, the last yielding preleptotene spermatocytes.…”

Section: What Is Known About the Cycle Of The Seminiferous Epithelium?mentioning

confidence: 88%

“…For those competent in French or German, early papers still provide fascinating reading (see citations in Roosen-Runge, 1962;Clermont, 1967). ''Modern'' study of human spermatogenesis was pioneered by Rosen-Runge (1952, 1956, Clermont and Leblond (1955), Clermont (1963), and Clermont (1963, 1964).…”

Section: Rupert P Amannmentioning

confidence: 99%

The Cycle of the Seminiferous Epithelium in Humans: A Need to Revisit?

Amann¹

2008

Journal of Andrology

271

167

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Understanding the dynamics of spermatogenesis is central to clinical andrology or to probing environmental effects on human testes. This review considers what is known about renewal and proliferation of spermatogonia, how germ cells are organized in cellular associations constituting the cycle of the seminiferous epithelium, relative frequencies of cellular associations, durations of the cycle of the seminiferous epithelium and spermatogenesis, and measurement of daily sperm production. Daily sperm production (DSP) per testis tends to decline with advancing age. Regardless of age, there is substantial loss of potential sperm from degeneration of spermatocytes, but not spermatids. DSP per gram testis parenchyma or DSP per testis cannot be predicted on the basis of testis size or age of a man. The review shows why our 1960s data base is neither robust nor precise and suggests how deficiencies might be rectified. New cellular associations should be defined, with none representing .15% of the cycle of the seminiferous epithelium. Then determine when A pale -spermatogonia become committed to proliferate or how many mitotic divisions occur thereafter. Restudy the duration of spermatogenesis because the accepted value might be in error by ,6 days. Restudying human spermatogenesis will benefit clinicians, toxicologists, and epidemiologists probing testis function by direct evaluations or indirectly via evaluations of quantity and quality of sperm ejaculated. It also will benefit scientists interested in renewal and proliferation of spermatogonia, or a spermatogonium as a prototype stem cell.

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Quantitative Investigations on Human Testicular Biopsies

Cited by 25 publications

References 5 publications

Role of compensatory meiosis mechanisms in human spermatogenesis

Role of compensatory meiosis mechanisms in human spermatogenesis

Studies of Testicular and Epididymal Damage in Relation to the Occurrence of Antisperm Antibodies

The Cycle of the Seminiferous Epithelium in Humans: A Need to Revisit?

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