Biomedical subjects

T Diemer

Publications and source records attributed to T Diemer.

26 records · Page 2Linked to original sources

PubMed2000

Influence of urogenital infection on sperm function.

Male accessory sex gland infections are considered to be hazards to male fertility. Various pathophysiologic concepts have evolved from experimental and clinical studies that begin to explain the effects of bacteria and immunologic events on spermatozoa. Recent studies have identified and evaluated mediators that are responsible for specific molecular processes in infections that particularly affect the function of spermatozoa.

Bacterial Infections↗

PubMed2000

Diametric effects of bacterial endotoxin lipopolysaccharide on adrenal and Leydig cell steroidogenic acute regulatory protein.

Immune activation results in the activation of adrenal steroidogenesis and inhibition of gonadal steroidogenesis. Previous studies indicated that these effects were caused primarily by activation and suppression of the secretion of ACTH and LH, respectively. However, other evidence indicated a direct effect of the immune system on the gonads. In this study, serum testosterone, quantitated by RIA after lipopolysaccharide injection, showed a significant decrease within 2 h. Parallel measurement of serum LH showed no change. There were no differences in LH receptor or cAMP produced in Leydig cells between vehicle- and lipopolysaccharide-injected mice. The 30-kDa form of the steroidogenic acute regulatory (StAR) protein was quantitated, by Western blot, in Leydig cells and was found to decrease in a time-dependent manner. No change in StAR protein messenger RNA (mRNA) was detected by Northern analysis during this time, nor were any changes found in the levels of mRNA for the steroidogenic enzymes P450scc, 3beta-hydroxysteroid dehydrogenase delta4-delta5-isomerase, or P450c17. In the adrenal, StAR protein was increased, as was StAR protein mRNA. No changes were observed in the levels of mRNA for P450scc, 3beta-hydroxysteroid dehydrogenase delta4-delta5-isomerase, or P450c21. Thus, although the mechanisms of regulation differ, changes in the levels of StAR protein are a sensitive indicator of the steroidogenic capacity of these two tissues.

3-Hydroxysteroid Dehydrogenases↗

PubMed1999

Role of cytokines in testicular function.

Inflammatory disease has been established to affect male reproductive function and fertility. Relevant inflammatory diseases include general and chronic infectious diseases as well as localized acute or chronic infections of the male genitourinary tract. Male accessory gland infections account for almost 15% of all cases of male infertility seen in infertility clinics while fertility usually is not a clinical objective among patients with acute systemic infections such as Gram-negative sepsis. Infections of the male accessory glands frequently are associated with increased counts of white blood cells in semen and elevated levels of proinflammatory cytokines in semen and the testis. There is a mounting body of evidence that demonstrates the importance of cytokines and chemokines in the regulation of testicular and glandular function during pathophysiological states as well as under normal physiological conditions when cytokines act as growth and differentiation factors. The purpose of this review is to examine the role of cytokines in the regulation of steroidogenesis and spermatogenesis in the testis under physiological and pathophysiological conditions and considers clinical investigations that help to improve the evaluation and treatment of male infertility.

Animals↗

PubMed1998

Influence of different uropathogenic microorganisms on human sperm motility parameters in an in vitro experiment.

The influence of different uropathogenic microorganisms (E. coli, enterococcus, Pseudomonas aeruginosa, Staphylococcus saprophyticus, Candida albicans) on human sperm motility was studied in vitro with a computer-assisted sperm analyser (CASA). Native ejaculates were prepared with the swim-up technique and adjusted to 22 x 10(6) spermatozoa ml-1. The sperm suspension was artificially infected with microorganisms in concentrations varying from 2 x 10(3) to 2 x 10(7). Sperm motility was examined directly after incubation, 2, 4 and 6 h later using the Mika motion analysis, a computer-based, automatic motility analysis. Former results with E. coli (serotype 06) could be confirmed that a significant inhibitory effect on sperm motility was associated with bacterial growth. Experiments with the enterococcus strain and Staphylococcus saprophyticus indicated no significant influence on sperm motility parameters. Tests with Pseudomonas aeruginosa showed a decrease of progressive motility according to time, but not to different bacterial concentrations. A significant inhibitory effect of Candida albicans was only detected in the samples with the initial bacterial concentration of 2 x 10(7) microorganisms ml-1.

Bacteria↗

PubMed1996

Influence of Escherichia coli on motility parameters of human spermatozoa in vitro.

The influence of E. coli on human sperm motility was studied in vitro. Semen samples were prepared by a swim-up technique and adjusted to 22 x 10(6) spermatozoa/ml. Samples were then inoculated with different concentrations of a uropathogenic strain of E. coli, serotype 06, with initial sperm/bacteria ratios varying between 10:1 and 10000:1. Motion parameters were analysed by computer-aided motility analysis directly, and 2, 4 and 6 h after inoculation. In a second series of experiments, bacterial replication was inhibited by addition of chloramphenicol. In a third series, the effect of E. coli culture filtrates on sperm motility was investigated. The direct inhibitory effect of E. coli on progressive motility of spermatozoa was found to depend upon the bacterial concentration. A distinct inhibitory effect was observed only at a sperm/bacteria ratio of approximately 1, achieved by growth of E. coli during the experiments. For modality of motion, no distinct changes were observed. When growth of bacteria was prevented by chloramphenicol, no inhibitory effect on sperm motility was detected. Sperm motility was not inhibited by E. coli culture filtrates. Analysis by electron microscopy revealed multiple adhesions of E. coli to spermatozoa, causing variable ultrastructural damage as probable morphological correlates of immobilization.

Bacterial Adhesion↗

PubMed1994

[Infections of the ejaculate by sexually transmissible pathogens].

Certain ejaculate infections can be traced back to sexually transmitted microorganisms, such as Neisseria gonorrhoeae, Chlamydia trachomatis, Ureaplasma urealyticum and Trichomonas vaginalis. To varying extents, these microorganisms cause such classical genital infections as urethritis, epididymitis and prostatitis as well as subclinical genital tract infections. Several different pathomechanisms are under discussion for infection of the ejaculate: reduction of spermatogenesis resulting from testicular damage, autoimmune processes induced by inflammation, direct influence on the spermatozoal function, disturbances in spermatozoal transport, secretory dysfunction of the male accessory sex glands and leukocytospermia with secondary influence on ejaculate parameters. The relevance of these microorganisms for the localization of the inflammatory process within the genital tract are discussed in detail. Their importance for male fertility is a matter of debate. In particular, the significance of C. trachomatis and U. urealyticum, both of which are detectable in the urethra, is still uncertain and cannot be assessed conclusively. Further information allowing delimitation of an infection resulting from bacterial colonization may be provided, on the one hand, by biochemical markers for an inflammatory reaction and indicators of an immune response in the ejaculate, e.g. PMN elastase, complement C3, or coeruloplasmin, and on the other hand, by secretion markers such as alpha-glucosidase, PSA and phosphatase. Whether the assessment of these markers and indicators can help to clarify the inflammatory origin of infertility in individual cases remains doubtful.

Acute-Phase Proteins↗

PubMedDate not supplied

Developmental and genetic disorders in spermatogenesis.

The most common cause of male infertility is idiopathic. Fresh insights based on genetic and molecular analysis of the human genome permit classification of formerly unexplained disorders in spermatogenesis. In this article, we review new procedures that expand diagnostic and therapeutic approaches to male infertility. Recombinant DNA technology makes it possible to detect specific chromosomal and/or genetic defects among infertile patients. The identification of genes linked to disorders in spermatogenesis and male sexual differentiation has increased exponentially in the past decade. Genetic defects leading to male factor infertility can now be explained at the molecular level, even though the germ cell profile of infertile patients is too variable to permit classification of the clinical phenotype. Increasing knowledge of genes that direct spermatogenesis provides important new information about the molecular and cellular events involved in human spermatogenesis. Molecular analysis of chromosomes and/or genes of infertile patients offers unique opportunities to uncover the aetiology of genetic disorders in spermatogenesis. Increasing numbers of cases, previously classified as idiopathic, can now be diagnosed to facilitate the treatment of infertile men. Advanced knowledge also poses ethical dilemmas, since children conceived with assisted reproductive technologies such as intracytoplasmic sperm injection (ICSI) are at risk for congenital abnormalities, unbalanced complements of chromosomes and male infertility.

Chromosome Aberrations↗

PubMedDate not supplied

Percoll density gradient centrifugation and consecutive flow cytometry do not identify leukocytes and leukocyte subtypes in ejaculate specimens.

This paper describes an attempt to establish a new combined method of leukocyte analysis in human ejaculate by Percoll density gradient centrifugation and consecutive flow cytometry. As a first step, leukocyte separation was performed by Percoll density gradient centrifugation with consecutive enrichment of leukocytes, especially granulocytes, in the 40%/60% and 60%/80% Percoll interfaces. Then these fractions were stained with specific monoclonal antibodies and analysed in a Facscan flow cytometer. Flow cytometric analysis did not demonstrate identifiable leukocyte populations, indicating a questionable cross-reaction with spermatozoal elements. Therefore, the combined technique of Percoll density gradient centrifugation and flow cytometric analysis were considered unsuitable for clinical leukocyte determination.

Antibodies, Monoclonal↗