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C Chubb

Publications and source records attributed to C Chubb.

18 recordsLinked to original sources
PubMed1992

Genes regulating testis size.

The studies described here provide information about the genetic and morphological bases for the significant differences in testis size among three closely related C57BL mouse substrains: C57BL/6J, C57BL/6ByJ, and C57BL/10J. C57BL/6J mice have normal-size testes while the other two substrains have small-size testes. Genes controlling testis size are postulated to be among the estimated forty genes that differ between the C57BL/6J and C57BL/6ByJ substrains. The number of genes involved in testis size regulation was examined using recombinant inbred mouse strains. An investigation of the role of Y chromosome genes was performed by completing molecular analyses with a mouse Y chromosome-specific probe. Sertoli and germ cell counts provided insight into the morphological basis for the different testis sizes. The experimental results suggest that there are at least two autosomal testis-size genes and that they control testis size by regulating the number of Sertoli cells.

Animals↗
PubMed1989

Texture interactions determine perceived contrast.

For a patch of random visual texture embedded in a surrounding background of similar texture, we demonstrate that the perceived contrast of the texture patch depends substantially on the contrast of the background. When the texture patch is surrounded by high-contrast texture, the bright points of the texture patch appear dimmer, and simultaneously, its dark points appear less dark than when it is surrounded by a uniform background. The induced reduction of apparent contrast is greatly diminished when (i) the texture patch and background are filtered into nonoverlapping spatial frequency bands or (ii) the texture patch and background are presented to different eyes. Our results are unanticipated by all current theories of lightness perception and point to a perceptual mechanism for contrast gain control occurring at an early cortical or precortical neural locus.

Contrast Sensitivity↗
PubMed1988

Drift-balanced random stimuli: a general basis for studying non-Fourier motion perception.

To some degree, all current models of visual motion-perception mechanisms depend on the power of the visual signal in various spatiotemporal-frequency bands. Here we show how to construct counterexamples: visual stimuli that are consistently perceived as obviously moving in a fixed direction yet for which Fourier-domain power analysis yields no systematic motion components in any given direction. We provide a general theoretical framework for investigating non-Fourier motion-perception mechanisms; central are the concepts of drift-balanced and microbalanced random stimuli. A random stimulus S is drift balanced if its expected power in the frequency domain is symmetric with respect to temporal frequency, that is, if the expected power in S of every drifting sinusoidal component is equal to the expected power of the sinusoid of the same spatial frequency, drifting at the same rate in the opposite direction. Additionally, S is microbalanced if the result WS of windowing S by any space-time-separable function W is drift balanced. We prove that (i) any space-time-separable random (or nonrandom) stimulus is microbalanced; (ii) any linear combination of pairwise independent microbalanced (respectively, drift-balanced) random stimuli is microbalanced and drift balanced if the expectation of each component is uniformly zero; (iii) the convolution of independent microbalanced and drift-balanced random stimuli is microbalanced and drift balanced; (iv) the product of independent microbalanced random stimuli is microbalanced; and (v) the expected response of any Reichardt detector to any microbalanced random stimulus is zero at every instant in time. Examples are provided of classes of microbalanced random stimuli that display consistent and compelling motion in one direction. All the results and examples from the domain of motion perception are transposable to the space-domain problem of detecting orientation in a texture pattern.

Fourier Analysis↗
PubMed1988

The fertility of hypothyroid male mice.

Male mice homozygous for the hypothyroid gene mutation were compared with normal siblings to determine whether hypothyroidism induced infertility by impairing sexual behaviour. In addition, the fertility of the hypothyroid mice was examined. The experimental results provide unequivocal evidence that genetically-induced hypothyroidism in male mice does not impair sexual behaviour or cause infertility.

Animals↗
PubMed1987

Impotence induced by a single gene mutation.

Inbred male mice homozygous for the stubby gene mutation were reported to be sterile nineteen years ago. However, the basis of the sterility has not been identified since testicular steroidogenesis and spermatogenesis are normal. In the present studies, the sexual behavior of stubby mice and their coisogenic, normal siblings was compared quantitatively. The experimental observations provided unequivocal evidence that the phenotypic basis of the sterility of stubby mice is impotency. Stubby mice represent the first animal model for the study of impotence and provide the first evidence of an autosomal gene mutation that has a primary effect on male sexual behavior.

Animals↗
PubMed1987

Mouse hybrid sterility and testicular function.

Crosses of BALB/c female mice and inbred wild male mice (PWD, PWK) produce fertile female progeny, but the male offspring are sterile. The hybrid male sterility is a direct action of the hybrid sterility genes Hst-1s and Hstws. Previous reports concluded that spermatogenic arrest effected the sterility. However, the testicular steroidogenesis of hybrid sterile male mice has not been elucidated. In the present report, the steroidogenic capacity of hybrid sterile and parental strain males was directly assessed by quantifying testosterone secretion by maximally stimulated testes perfused in vitro. Additionally, Leydig cell mass and germ cell volumes were morphometrically determined. The experimental results confirm the deleterious impact of the Hst-1s/Hstws genotype on spermatogenesis and demonstrate for the first time that the steroidogenic capacity of hybrid sterile testes is reduced. The biochemical defects that cause the impairment of testicular function are unknown.

Animals↗
PubMed1987

Sexual behavior and fertility of little mice.

Male mice homozygous for the little gene mutation (lit) were originally reported to have a marked incidence of infertility. We have previously reported that these diminutive mice have normal spermatogenesis and testicular steroidogenesis. In the present study, one research goal was to determine if the reported infertility was due to a defect in male sexual behavior. Quantitative analyses of male sexual behavior of little mice and their normal siblings were completed. Natural breeding trials were also performed to reexamine the fertility of little male mice. The experimental results suggested that little mice require significantly longer times for the first mount, first intromission, and ejaculation. More importantly, the investigation provided evidence that the little mice were not infertile but that they were subfertile. The diminutive size of the little mice may be the primary etiological factor for the observed subfertility.

Animals↗
PubMed1987

Animal models of physiologic markers of male reproduction: genetically defined infertile mice.

The present report focuses on novel animal models of male infertility: genetically defined mice bearing single-gene mutations that induce infertility. The primary goal of our investigations was to identify the reproductive defects in these mutant mice. The phenotypic effects of the gene mutations were deciphered by comparing the mutant mice to their normal siblings. Initially testicular steroidogenesis and spermatogenesis were investigated. The physiologic markers for testicular steroidogenesis were steroid secretion by testes perifused in vitro, seminal vesicle weight, and Leydig cell histology. Spermatogenesis was evaluated by the enumeration of homogenization-resistant sperm/spermatids in testes and by morphometric analyses of germ cells in the seminiferous epithelium. If testicular function appeared normal, we investigated the sexual behavior of the mice. The parameters of male sexual behavior that were quantified included mount patency, mount frequency, intromission latency, thrusts per intromission, ejaculation latency, and ejaculation duration. Females of pairs breeding under normal circumstances were monitored for the presence of vaginal plugs and pregnancies. The patency of the ejaculatory process was determined by quantifying sperm in the female reproductive tract after sexual behavior tests. Sperm function was studied by quantitatively determining sperm motility during videomicroscopic observation. Also, the ability of epididymal sperm to function within the uterine environment was analyzed by determining sperm capacity to initiate pregnancy after artificial insemination. Together, the experimental results permitted the grouping of the gene mutations into three general categories. We propose that the same biological markers used in the reported studies can be implemented in the assessment of the impact that environmental toxins may have on male reproduction.

Animals↗
PubMed1987

Efficacy of perfluorodecalin as an oxygen carrier for mouse and rat testes perfused in vitro.

Perfluorodecalin is a superior artificial oxygen carrier because of its high oxygen dissolving capacity, low toxicity, and short retention times within tissues. However, the instability of perfluorodecalin emulsions has hindered its application in blood substitutes. The present study addressed two questions. First, is perfluorodecalin deleterious to the endocrine function of testes? This question was examined by comparing testosterone secretion by testes perfused in vitro with medium incorporating either perfluorodecalin or erythrocytes as oxygen carriers. Second, can stable emulsions of perfluorodecalin be attained with the new surfactant Butronic U-1? This question was approached by determining the stability of perfluorodecalin emulsions containing either Butronic U-1 or Pluronic F-68, a proven ineffective surfactant. The experimental results support the efficacy of perfluorodecalin emulsions as oxygen carriers for mouse and rat testes perfused in vitro. Perfluorodecalin emulsions formed with Butronic U-1 were stable during the 4-hr perfusions but not during long-term storage.

Animals↗
PubMed1985

Reversal of the endocrine toxicity of commercially produced perfluorochemical emulsion.

Perfluorochemicals provide a biologically inert system for oxygen transport to tissue. The purpose of the present study was to determine if a simple clean-up procedure could reverse the endocrine toxicity of a commercially produced perfluorochemical emulsion, Oxypherol-E.T. The clean-up procedure consisted of a combined resin and dialysis treatment. The endocrine toxicity of the untreated and treated perfluorochemical emulsions was tested by determining their effect on testosterone secretion by rat testes perfused in vitro. Rat testes perfused with untreated Oxypherol-E.T. secreted low amounts of testosterone. However, the treated Oxypherol-E.T. was an effective and nontoxic oxygen carrier for testes perfused in vitro. The results are significant because they suggest that the endocrine toxicity of Oxypherol-E.T. is caused by toxic contaminants and not the perfluorochemicals. Additional experiments revealed that the fluoride ion may be the primary toxic contaminant of Oxypherol-E.T. The data support the efficacy of perfluorochemicals as oxygen carriers for rat testes perfused in vitro.

Animals↗
PubMed1985

Steroid secretion by rat testes perfused with perfluorochemicals as oxygen carriers.

Organs perfused in vitro are important experimental models for physiological studies. Perfusion medium supplemented with artificial oxygen carriers would at physiological flow rates supply sufficient oxygen to organs and would be superior to medium containing erythrocytes because it is more defined. Perfluorotributylamine (FC-43), a perfluorochemical, is an artificial oxygen carrier that has been previously reported to be ineffective in maintaining endocrine organs perfused in vitro. The purpose of this study was to determine the efficacy of FC-43 as an oxygen carrier for rat testes perfused in vitro. The effects of FC-43 on testicular function and structure were assessed by comparing the results of experiments using perfusion medium containing either FC-43 or erythrocytes. The results suggest that perfusion medium containing perfluorochemicals must be prepared by standardized procedures and defined as to its physiochemical parameters. The study resulted in the first successful in vitro perfusion of an endocrine organ with perfluorochemicals as oxygen carriers. The results not only provide the basis for an improved perfusion medium but also support in vitro perfused testes as effective experimental tools for testing perfluorochemical-based blood substitutes.

Animals↗
PubMed1985

Animal models of male infertility: mice bearing single-gene mutations that induce infertility.

Genetically defined mouse models of male infertility are described in the present report. The mice were rendered infertile by one of the following gene mutations: Ames dwarf, dwarf, flipper-arm, hightail, hypothyroid, little, pygmy, stubby. The effects of each gene mutation on testicular steroidogenesis and spermatogenesis were elucidated by a comparison of the mutant mice to their normal siblings. Testicular steroidogenesis was assessed directly by determining steroid secretion by testes perfused in vitro. The study provides the first comprehensive assessment of testicular function in the mutant mice. The eight gene mutations can be classified into two groups based on the results. One group of gene mutations (Ames dwarf, dwarf, flipper-arm, pygmy) specifically depress spermatogenesis and testicular steroidogenesis. The infertility of these mutant mice can be linked to the lowered total sperm production. The second group of gene mutations (hightail, hypothyroid, little, stubby) do not specifically depress either spermatogenesis or testosterone secretion. Subsequently, the etiology of the male infertility of the second group of mutant mice is unknown. We propose that these mutant mice provide valuable experimental tools for the study of male infertility and male reproduction.

Animals↗
PubMed1979

Steroid secretion by in vitro perfused testes: testosterone biosynthetic pathways.

Alternative metabolic pathways for the biosynthesis of testosterone from pregnenolone exist in mammalian testes. The following experiments were designed to identify the preferred testosterone biosynthetic pathway in rat and rabbit testes. The experimental protocol included the infusion of steroidogenic reaction inhibitors and testosterone biosynthetic intermediates into testes perfused in vitro. Under these conditions, the testicular steroid secretions were a measure of specific reaction activities. Infusion of medrogestone (6,17-dimethyl-4,6-pregnadiene-3,20-dione, Ayerst), an inhibitor of delta5-4isomerization, permitted the reactions converting pregnenolone to androstenediol to be studied separately from those converting progesterone to testosterone. For example, the activity of the pregnenolone vector 17alpha-hydroxypregnenolone reaction was measured as the total of the 17alpha-hydroxypregnenolone, dehydroepiandrosterone, and androstenediol secreted by medrogestone-inhibited testes. The reactions convering delta5-3beta-hydroxysteroids to delta4-3-ketosteroids were studied in testes infused with SU-10603 (7-chloro-3,4-dihydro-2-[3-pyridyl]-1(2H)-naphthalenone. Ciba-Geigy), an inhibitor of 17alpha-hydroxylation and C-17, C-20 cleavage reactions. The results indicated that preferred testosterone biosynthetic pathways are present and different in rat and rabbit testes.

Animals↗
PubMedDate not supplied

Genetically defined mouse models of male infertility.

The review has four objectives. The first objective is to summarize our studies of gene mutations that induce infertility in male mice. The second objective is to stress the power of mouse genetics and its application to male reproductive biology. The third objective is to provide useful references to the literature about gene mutations affecting male mouse fertility. Our goal is to cite references that can be used as a starting point for reading, not to present a comprehensive list of references. The fourth objective is to present a summary of selected data collected from mice representing 21 mouse strains.

Animals↗
PubMedDate not supplied

Oligotriche and quaking gene mutations. Phenotypic effects on mouse spermatogenesis and testicular steroidogenesis.

The phenotypic actions of the oligotriche gene mutation on testicular function have not been elucidated, although it is known that male mice homozygous for the mutation are infertile. In the present study, the effect of the oligotriche gene mutation on mouse testicular function was analyzed by comparing normal and mutant mice. Spermatogenesis was analyzed by enumerating germ cells in seminiferous tubules at specific stages of spermatogenesis and by electron microscopy. Steroidogenic potential was estimated by radioimmunometric determination of testosterone secreted by testes perfused in vitro. Parallel studies were completed for male mice homozygous for the quaking gene mutation, a mutation known to cause male mouse sterility by disrupting sperm tail development. The experimental results suggest that the oligotriche and quaking gene mutations interfere with sperm tail formation by different mechanisms. Testicular steroidogenesis was not affected by either gene mutation. The results provide the first evidence that the oligotriche gene mutation induces male mouse sterility by effecting the complete absence of a sperm tail. This phenotypic action is different from that of the quaking gene mutation.

Animals↗