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Results for “testis development”

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At least 1,405 records · Page 78Linked to original sources
PubMed1994

Left sided abdominal pain in childhood.

In a paediatric surgical practice over a 10 year period, 59 children presenting with left sided abdominal pain, acute or chronic, were investigated and followed up to identify the cause. Only two were found to have an identifiable surgically significant cause, one being hydronephrosis and the other being congenital uterine abnormality. Other causes suspected were Mittelschmerz, faecal retention or gastroenteritis, functional, abdominal migraine and allergy. Two boys developed torsion of the testis within 2 years of an episode of left sided abdominal pain. This is considered significant and the examination of boys with left sided abdominal pain should include careful scrutiny of the testis and assessment of its disposition with the boy standing. In both sexes investigation should focus initially on the urinary tract.

Abdominal Pain↗
PubMed1983

Effect of dietary linoleic and linolenic acids on testicular development in the rat.

In two experiments a total of twelve male rats were reared from weaning for up to 63 weeks on an essential fatty acid (EFA)-deficient diet alone (2 X two animals) or supplemented with the methyl esters of linoleic acid (18:2 omega 6) (2 X two animals) or linolenic acid (18:3 omega 3) (2 X two animals). Testicular development was normal in rats given 18:2 omega 6, but in rats fed the EFA-deficient diet alone, and in those supplemented with 18:3 omega 3 the testes were reduced in size. Histologically, a degeneration of the seminiferous tubules was noted, with progressive loss of the germinal cells, and with an absence of spermatozoa in the lumina of the seminiferous tubules and epididymides. Leydig cells appeared unaffected, and were prominent. The six rats in Experiment 1 were capable of mating with females reared on commercial diets, but only the two 18:2 omega 6 supplemented animals were fertile. There was a marked reduction in the percentage of arachidonic acid (20:4 omega 6) and docosapentaenoic acid (22:5 omega 6) in the total fatty acids of the atrophic testes. There was no compensatory increase in long-chain derivatives of 18:3 omega 3 in the 18:3 omega 3 fed rats and it is concluded that linolenic acid cannot replace linoleic acid in the development of the rat testis.

Animals↗
PubMed1980

Abnormality of the X chromosome in human 46,XY female siblings with dysgenetic ovaries.

An abnormal extra band was found on the short arm of the X chromosome in a 46,XY female and in her 46,XY female fetal sibling. Despite presence of the intact Y chromosome, there was no evidence of testicular differentiation in either subject. Production of H-Y antigen was suppressed in both subjects. The data suggest that development of the mammalian testis requires a normal function of the X chromosome.

Female↗
PubMed1997

Human estrogen receptor beta-gene structure, chromosomal localization, and expression pattern.

The estrogen receptor (ER) is a ligand-activated transcription factor that mediates the effects of the steroid hormone 17 beta-estradiol, in both males and females. Since the isolation and cloning of ER, the consensus has been that only one such receptor exists. The finding of a second subtype of ER (ER beta) has caused considerable excitement amongst endocrinologists. In this article, we present data regarding the genomic structure and chromosomal localization of the human ER beta gene, demonstrating that two independent ER genes do exist in the human. Furthermore, we present data regarding the tissue distribution of human ER beta, showing that this receptor is expressed in multiple tissues. For instance, ER beta is found in developing spermatids of the testis, a finding of potential relevance for the ongoing debate on the effects of environmental estrogens on sperm counts. In addition, we find ER beta in ovarian granulosa cells, indicating that estrogens also participate in the regulation of follicular growth in the human.

Amino Acid Sequence↗
PubMed1995

Gestational and lactational exposure of rats to xenoestrogens results in reduced testicular size and sperm production.

This study assessed whether exposure of male rats to two estrogenic, environmental chemicals, 4-octylphenol (OP) and butyl benzyl phthalate (BBP) during gestation or during the first 21 days of postnatal life, affected testicular size or spermatogenesis in adulthood (90-95 days of age). Chemicals were administered via the drinking water or concentrations of 10-1000 micrograms/l (OP) or 1000 micrograms/l (BBP), diethylstilbestrol (DES; 100 micrograms/l) and an octylphenol polyethoxylate (OPP; 1000 micrograms/l), which is a weak estrogen or nonestrogenic in vitro, were administered as presumptive positive and negative controls, respectively. Controls received the vehicle (ethanol) in tap water. In study 1, rats were treated from days 1-22 after births in studies 2 and 3, the mothers were treated for approximately 8-9 weeks, spanning a 2-week period before mating throughout gestation and 22 days after giving birth. With the exception of DES, treatment generally had no major adverse effect or body weight: in most instances, treated animals were heavier than controls at day 22 and at days 90-95. Exposure to OP, OPP, or BBP at a concentration of 1000 micrograms/1 resulted in a small (5-13%) but significant (p < 0.01 or p < 0.0001) reduction in mean testicular size in studies 2 and 3, an effect that was still evident when testicular weight was expressed relative to body, weight or kidney weight. The effect of OPP is attributed to its metabolism in vivo to OP. DES exposure caused similar reductions in testicular size but also caused reductions in body weight, kidney weight, and litter size. Ventral prostate weight was reduced significantly in DES-treated rats and to minor extent in OP-treated rats. Comparable but more minor effects of treatment with DES or OP on testicular size were observed in study 1. None of the treatments had any adverse effect on testicular morphology or on the cross-sectional area of the lumen or seminiferous epithelium at stages VII-VIII of the spermatogenic cycle, but DES, OP, and BBP caused reductions of 10-21% (p < 0.05 to p < 0.001) in daily sperm production. Humans are exposed to phthalates, such as BBP, and to alkylphenol polyethoxylates, such as OP, but to what extent is unknown. More detailed studies are warranted to assess the possible risk to the development of the human testis from exposure to these and other environmental estrogens.

Animals↗
PubMed1993

Postnatal development of testicular cell populations in mice.

The postnatal development of body and testis weight and the size of the testicular cell populations were studied in CBA mice up to day 52 post partum. The body weight increased from 1.3 g at day 1 to 22.5 g at day 52. Over the same interval the testis weight showed a faster increase from about 1 mg to almost 60 mg. Spermatogenesis was found to be complete by day 35. The numbers of A spermatogonia, Sertoli cells, Leydig cells, mesenchymal cells, macrophages, myoid cells, lymphatic endothelial cells, endothelial cells and perivascular cells per testis were studied from day 3 to day 50, using the dissector method. The number of A spermatogonia increased from 0.2 x 10(5) at day 3 to 6.5 x 10(5) at day 21 and remained more or less constant thereafter. The Sertoli cell population increased during the first three weeks after birth to reach the adult level of approximately 18 x 10(5) cells per testis. In the interstitium the Leydig cells showed a sharp increase between days 11 and 31 followed by a small decrease to ultimately 9 x 10(5) cells per testis. The Leydig cells formed 8% of the total number of interstitial cells per testis at day 11, increasing to 30% at day 50. The number of mesenchymal cells did not change until day 36, decreasing thereafter from about 2.5 x 10(5) to 1 x 10(5) cells per testis at day 50. However, the percentage of the total number of interstitial cells that were mesenchymal cells decreased from 59% to 4%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Urogenital infection and seminal excretion after inoculation of bulls and rams with chlamydiae.

Five mature rams and 4 bulls were inoculated parenterally with bovine or ovine chlamydial strains of type 1 and 2. One to 3 days later, all animals developed a chlamydemia lasting 4 to 8 days. Chlamydial agents were isolated from the semen near the end of the chlamydemic phase. All rams and 3 of 4 inoculated bulls excreted chlamydiae in the semen for 22 to 29 days. From 8 to 39 days after inoculation, selected rams or bulls were killed to test for chlamydial infection in the urogenital tract and other organs. Chlamydiae were isolated in developing chicken embryos from testis, epididymis, and accessory sex glands. Bulls examined 29 and 39 days after inoculation did not harbor chlamydiae. Chlamydiae were also not isolated from 3 control bulls which were from the same herd as the principal bulls. All inoculated bulls and rams had a group-specific chlamydial antibody response within 7 days. The titers reached maximal levels of 128 to 512 at 14 days after inoculation. Subsequently, the antibody titers decreased gradually. Seminal plasma collected at different times after animals were inoculated did not fix complement in the presence of chlamydial group antigen. The number of polymorphonuclear leukocytes in the semen increased during the experiment. The semen was grossly purulent in 2 rams inoculated with the type 2 chlamydial strain of polyarthritis.

Animals↗
PubMed1990

Increased levels of junB and c-jun mRNAs in male germ cells following testicular cell dissociation. Maximal stimulation in prepuberal animals.

We have examined the relative transcript levels of the junB and c-jun proto-oncogenes during development of the mouse testis. junB and c-jun mRNA levels are low in total RNA from intact immature or mature testes. Dissociation of testicular cells, however, increases the levels of junB and c-jun mRNAs, with higher increases in the dissociated cells from testes of 8-day-old mice than from 17-day-old or sexually mature mice. These differences in junB and c-jun mRNA levels localize to specific cell types. In testes from 8-day-old mice, the mRNA levels for both proto-oncogenes are higher in type B spermatogonia and in the interstitial cell fraction than in type A spermatogonia. In testes of 17-day-old mice, the highest mRNA levels for both proto-oncogenes are seen in preleptotene spermatocytes and interstitial cells, with decreasing levels in leptotene/zygotene spermatocytes and prepuberal pachytene spermatocytes. junB and c-jun mRNAs are nearly undetectable in pachytene spermatocytes, round spermatids, and residual bodies/cytoplasts. The increased junB mRNA levels originate not only from the expected 2.1-kilobase transcript but from a more slowly migrating transcript of about 2.3 kilobases. RNase H analysis demonstrates that this migration change was due to an increase in mRNA polyadenylation. The low levels of junB and c-jun mRNAs in intact testes and the much higher levels in isolated cells from identical testes suggest that the disruption of cell-to-cell contact increases the amount of junB and c-jun transcripts in specific cells of the testis. Coupled with this increase, structural changes are seen with the junB mRNA.

Animals↗
PubMed1979

[Epididymal and testicular metastases. 2 cases (author's transl)].

Two cases of epididymotesticular metastases are reported: one epididymal from a carcinoma of the kidney by retrograde venous spread and the other testicular secondary to a carcinoma of the prostate and apparently by arterial spread. Epididymotesticular metastases of carcinomas are rare. When the initial carcinoma is known, or even treated, the development of a large testis should lead to consideration of the possibility. Treatment should consist of inguinal orchidectomy with ligation of the spermatic cord as high as possible.

Adenocarcinoma↗