Sex differences in thrombosis are well described, but their underlying mechanism(s) are not completely under- stood. Coagulation proteins are synthesized in the liver, and liver gene expression is sex specific and depends on sex differences in growth hormone (GH) secretion — males secrete GH in a pulsatile fashion, while females secrete GH continuously. Accordingly, we tested the hypothesis that sex-specific GH secretion patterns cause sex differences in thrombosis. Male mice were more susceptible to thrombosis than females in the thrombo- plastin-induced pulmonary embolism model and showed shorter clotting times ex vivo. GH-deficient little (lit) mice were protected from thrombosis, and pulsatile GH given to lit mice restored the male clotting phe- notype. Moreover, pulsatile GH administration resulted in a male clotting phenotype in control female mice, while continuous GH caused a female clotting phenotype in control male mice. Expression of the coagulation inhibitors Proc, Serpinc1, Serpind1, and Serpina5 were strongly modulated by sex-specific GH patterns, and GH modulated resistance to activated protein C. These results reveal what we believe to be a novel mechanism whereby sex-specific GH patterns mediate sex differences in thrombosis through coordinated changes in the expression of coagulation inhibitor genes in the liver.
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Here we explored a highly specialised host-ectoparasite system investigating sex ratio, aggregation and host pref- erence of parasitic bat flies. Using an extensive sample size of both host and their parasites, collected using thorough and objective methodology we reached three important conclusions. First, we showed that contrary to previous knowledge  bat fly sex ratios are highly variable among hosts and we demonstrate that this vari- ation is strongly associated with infrapopulation size. Bat flies exhibit strongly male-biased sex ratios in small, and strongly female-biased sex ratios in large infrapopula- tions, indicating sex-specific aggregation. This finding contradicts predictions of the local mate competition and appears to be rather the result of sex-specific host- preference, mobility or competitive ability. Secondly, we showed that parasites aggregate in larger numbers on female hosts, and parasite abundance increased with increasing host body condition. Given the high transmis- sibility of bat flies, these results arguably reflect parasite preference for these host traits. Thirdly, we demon- strated that the latter associations are the results of female, but not male bat fly preference for host traits. We argue that this sex-specific preference for host traits is probably the driving force of the density-dependent sex ratio bias across infrapopulations in this host- parasite system.
Sex-specific effects of maternal prenatal stress on birth outcomes have also been reported. Prior work suggests that female fetuses differentially adapt to intrauterine stressors by decreasing growth rates. A study in Israel of chronic maternal stress found that female fetuses were at increased risk for preterm birth and low birth weight . Similarly, in Chile, maternal prenatal exposure to a negative life event was associated with a reduction in gestational age and increased risk of preterm birth, espe- cially in girls . Females may have increased HPA axis reactivity and female placentas may increase permeabil- ity to glucocorticoids following maternal stress, as com- pared to males . Sex-specific differences in placental gene expression and immune function have also been described [15, 16].
(including humans) (Gonzalez et al., 2007; Kato et al., 1998; Resko & Roselli, 1997; Wallen, 2005), the distribution of which is highly conserved in vertebrates (Brandenberger, Tee, Lee, Chao, & Jaffe, 1997; Cao & Patisaul, 2013; MacLusky, Chaptal, & McEwen, 1979; Walker, Juenger, & Gore, 2009). Thus, perturbation of neonatal ESR expression by BPA exposure could be a mechanism by which the steroid hormone–dependent organization of these subregions is altered. Moreover, very little is known regarding the impact of prenatal-only BPA exposure on brain sexual differentiation, so the results presented here yield new insights regarding effects resulting from this specific exposure window. Because BPA has long been regarded as estrogenic (Dodds, Goldberg, Larson; W., & Robinson, 1938), and prenatal estrogen exposure is masculinizing in female rodents (McCarthy, 2008), ethinyl estradiol (EE) was used as a reference estrogen. Understanding and elucidating the pathways and critical periods in which the vulnerabilities to, and consequences of, low-dose BPA exposure manifest in animal models will contribute mechanistic knowledge requisite to evaluate the potential risk of BPA exposure in humans.
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Table 2. Wald F-test results for terms in linear mixed effects models evaluating morphological differences between Gallotia galloti in different environments and between sexes on Tenerife. When the ENV×SEX interaction was not significant (α = 0.05), a reduced model was fitted. All tests are based on marginal sums of squares. The models for head size incorporated unequal variances among environment because AIC c indicated this provided better fit than assuming
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Hormones play an important role in developmental plasticity (Dufty et al., 2002; West-Eberhard, 2003). For example, steroids produced during embryonic development induce and regulate differences between the sexes in primary sexual characters, brains and behaviour (Adkins-Regan, 2005; Carere and Balthazart, 2007). This suggests that hormone production by embryos will be highly time and site specific and subject to strong selection to avoid production of inferior (for example, intermediate) phenotypes. However, embryos are also subject to hormone exposure from external sources, which may or may not be adaptive. In rodents, for example, a by-product of embryonic steroid production is that hormone leakage between foetuses can modify the absolute or relative hormone exposure of individual embryos (Ryan and Vandenbergh, 2002). Such variation in hormone exposure has been implied in causing morphological, physiological, behavioural and life-history variation among offspring in both mammals and viviparous lizards (reviewed by Clark and Galef, 1998; Ryan and Vandenbergh, 2002; Uller, 2006).
signaling-dependent deterioration of oocyte quality . A recent analysis of genes influencing reproductive span has indicated that contact with males influences reproductive as well as somatic aging  (also see section 3.3.). Males of C. elegans lose the ability to cross-fertilize by day 7 of adulthood, around 1/3 of their average lifespan, and this seems to reflect a declining ability to execute mating behavior that can be modulated by insulin signaling, rather than deterioration of gamete function . However, C. elegans males are dispensable for reproductive success, whereas in dioecious species the maintenance of male vigour has more bearing on fitness. Indeed, males of the dioecious nematode C. remanei maintain progeny production for longer and reach peak reproductive performance at a later age than females . A study in another dioecious species, P. exspectatus, found that changes in crawling speed, a proxy for somatic senescence, contributed to male but not female reproductive decline. This demonstrates some sex-specificity of the age-related mechanisms behind reproductive senescence and their interaction with somatic deterioration . Specifically, reproductive senescence in P. exspectatus males might, as in C. elegans, depend on diminished efficacy of mating behavior, or on some other male-specific activity such as mate search. Whether shared molecular mechanisms underlie sex-specific features of reproductive senescence largely remains to be determined.
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This issue is now being addressed in in vivo settings. Reports evaluating gametocyte clearance by anti-malar- ial drugs and sex specific densities could not find sig- nificant changes in gametocyte sex ratio [30, 89]. On the other hand, two recent clinical trials studied the effect of anti-malarial drugs on gametocyte sex ratio in vivo and concluded that treatments produced in both instances a shift in the gametocyte sex ratio. One clinical trial was conducted in Kenya with 120 infected children from an area of moderate malaria transmission. RT-qPCR assays amplifying the female marker pfs25 and the male marker pfGMET were used to measure the gametocyte sex ratio after a dihydroartemisinin-piperaquine treatment alone or combined with primaquine. In both cases male game- tocytes appeared to be cleared more slowly than females, resulting in a male shifted sex ratio . Another clini- cal trial was conducted in Mali on 80 infected males aged 5 to 55 from a hyperendemic, highly seasonal malarious region. The same assays were used to measure effect on gametocyte sex ratios of the addition of primaquine to a sulfadoxine-pyrimethamine and amodiaquine treatment and of the addition of methylene blue to a dihydroarte- misinin-piperaquine treatment. The significant decrease in overall gametocyte density associated in particular to the treatment with methylene blue was in this case asso- ciated with a strongly reduced circulation time of male gametocytes and an increased female sex ratio [32, 34].
Additional file 3: A. Number of differentially expressed (regulated) genes in each of the seven microarray comparisons. Each gene listed in this table meets the threshold requirements of a |fold change| > 1.5, p < 0.0001, and has a well above background intensity value for at least one of the seven microarray comparisons. The number of sex-specific genes greatly increased from 3 wk to 8 wk; also see Table 1. A larger number of genes changed from 3 or 4 wk to 8 wk in male liver compared to female liver. B. Detailed microarray data for each of the 5,715 regulated genes. Each gene listed in this table meets the threshold requirements as in Additional file 3A. Data shown include Rosetta-computed weighted ratios, Rosetta p-values, and microarray signal intensities for the 7 microarray experiments. The “ is well above background ” value column uses a binary value to identify arrays that met this requirement (score = 1), as well as arrays where this requirement was not met (score = 0.1 or 0.01), in which case the probe is considered as not meeting the threshold for significance for that array, irrespective of the fold-change and p-values shown. Stringent sex-independent genes meet the criteria of a |fold change| < 1.2, a p-value > 0.01, and a minimum intensity of 25. Genes that do not meet this criteria and do not meet the criteria of sex- specificity (|fold change| > 1.5 and p-value < 0.0001) are labeled as sex- independent. C. Developmental changes in expression during pre- pubertal period. The gene changes listed take into account the developmental changes occurring from both 3 wk to 8 wk and from 4 wk to 8 wk and are based on the TFS number assigned to each gene (Additional file 2). The most prominent developmental change observed was a change in male liver only. A larger percentage of genes displayed a developmental change in male liver (77%) than in female liver (53%). Additional file 4: A. Box and whisker plots representing gene expression
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Here, we analyzed genetic influence on eosinophil in- filtration after L. major infection into the lymph nodes of strains BALB/cHeA (BALB/c), STS/A (STS), and se- lected 12 (out of 20) RC strains of CcS/Dem series . Each of the 20 RC CcS/Dem strains contains a different unique set of approximately 12.5% genes of the donor strain STS on the genetic background of BALB/c. We found surprisingly high numbers of eosinophils in the inguinal lymph nodes of the strain CcS-9, males contain- ing higher numbers of eosinophils than females. We an- alyzed genetics of this infiltration using microsatellite DNA markers and mapped four loci that control eosino- phil numbers after L. major infection, one of them being strongly influenced by sex. We also found that the num- bers of eosinophils in the lymph nodes correlate posi- tively with the parasite load and that this correlation is partly genetically controlled and is higher in males than in females.
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20-months-old female and male C57BL/6N mice. Control animals underwent PBS treatment ( n = 7 – 11 animals/sex/ treatment). Animals were investigated for impact of sex on body weight, food and water intake, body temperature, heart rate, behaviour (locomotor activity, motor coordination and strength) and serum thyroid hormone (TH) status. Results: Distinct sex impact was found in eu- and hyperthyroid mice, while phenotypic traits of hypothyroidism were similar in male and female mice. No sex difference was found in TH status of euthyroid mice; however, T4 treatment resulted in twofold higher TT4, FT4 and FT3 serum concentrations in adult and old females compared to male animals. Hyperthyroid females consistently showed higher locomotor activity and better coordination but more impairment of muscle function by TH excess at adult age. Importantly and in contrast to male mice, adult and old hyperthyroid female mice showed increased body weight. Higher body temperature in female mice was confirmed in all age groups. No sex impact was found on heart rate irrespective of TH status in adult and old mice.
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differences in recombination rate between the sexes we ana- held in common with the male map. For comparison, lyzed the slopes of the lines by simple linear regression of two the calculated average of the lengths of the male and continuous variables (male and female) in groups defined as female maps [(m ⫹ f )/2] is 1762.6 cM. Thus, the sex- left, middle, and right thirds. The left-third data points in-
Second, independent of gene dose differences, sex chro- mosomes are also inherited unequally between the sexes, leading to distinct evolutionary forces relative to the auto- somes (Rice 1984; Charlesworth et al. 1987). In particular, conﬂicting selection on males and females results in unequal sex-speciﬁc selection pressures acting on the sex chromo- somes. This, in turn, inﬂuences rates of sequence and expres- sion evolution (Vicoso and Charlesworth 2009; Meisel and Connallon 2013). Older sex chromosome regions, where re- combination between the Z-W orthologs was halted earlier, have been exposed to these selection pressures for a greater period of time. This cumulative nature of sex-speciﬁc selection can lead to regional differences in sex-speciﬁc gene regulation based on regional age (Wright et al. 2012; Wang et al. 2014). The avian Z chromosome, which is conserved across all extant birds, is particularly interesting in the study of regional differences in sex-speciﬁc gene regulation. All avian species examined thus far show incomplete dosage compensation (Ellegren et al. 2007; Itoh et al. 2007; Wolf and Bryk 2011; Wright et al. 2012; Moghadam et al. 2013; Uebbing et al. 2013; Wang et al. 2014). As a result, most of the Z chromo- some exhibits male-biased expression (Ellegren et al. 2007). However, there is extensive variation in the degree of male bias in expression across the chromosome. Previous work in
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Results: Fifteen commonly used shoulder pain quality descriptors were identified. Among them, “sore” was the most frequently used, followed by “pulled”. Deep pain sensations (eg, sore, pulled, torsion, and taut) were relatively more predominant than superficial pain sensations (eg, pricking and lacerating). In terms of sex-related differences, female patients used more pain quality descriptors than the male patients (5.5 vs 3.7, P<0.001). The frequency of paroxysmal, dullness, and constriction-related pain quality descriptors, such as “shooting”, “faint”, “click- ing”, and “squeezing”, were higher in females than in males (all P<0.05).
the onset of puberty. These actions of sex hormones on metabolic homeostasis and their implication for diabetes and obesity in males and females have been extensively described in recent reviews and will not be discussed here [24, 52]. However, it is important to stress that non-reproductive organs like the brain and adipose tis- sue are also sites of androgen and estrogen biosynthesis. In these tissues, androgens convert to estrogens in both males and females. Adipose tissue is also a reservoir of sex steroids that act locally in a paracrine and intracrine manner (reviewed in ). The total sex steroid content of adipose tissue has been estimated in some studies to be a hundred times greater than total plasma content . Steroid fatty acid esters are present in adipose tissue of both male and female rats . These testosterone es- ters are long-lived in the blood even after castration and represent an adipose testosterone reservoir for slow re- lease (although human adipose tissue steroid ester has not yet been demonstrated). Further, tissue metabolism or in- activation of estrogen by the cytosolic enzyme estrogen sulfotransferase (EST) is also an essential factor in con- trolling cellular estrogenic action and sex differences in adipose biology; [56, 57]. Thus, in human adipose tissue (and in the brain), the local tissue and cellular output of sex hormone action is more complex than would be pre- dicted by simple measurement of serum sex hormone
The following conclusions can be reached (see also Table 1). (1) Sex is a variable in defining mechanisms responsible for cardiovascular structure and function in health and disease, and must be considered for all experimental designs and system choices (that is, cell culture, isolated tissues and whole animals, including genetically manipulated animals). (2) Phenotypes dic- tated by the sex chromosomes are modulated by sex steroid hormones; therefore, sex and hormonal status are critical in the design of experiments. (3) If differen- tial experimental results occur in animals based purely on sex, much can be gained by studying the ‘most affected ’ as well as the ‘ most protected ’ sex. (4) Studies in animals need to account for hormonal/gonadal status in both males and females (that is, intact, gonadecto- mized, sexually immature, hormone replete or replaced), as well as reproductive history of females. (5) Experi- ments that utilize both female and male animals should be sufficiently powered to detect sex difference if they exist or if not to provide confidence in a null finding, which should be reported. Analysis by sex includes sex as a dichotomous variable as well as a covariate. (6) As numerous studies have identified differential responses between sexes in etiology, consequences and treatment of cardiovascular disease, the idea that studies of
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In 1990s,it becomes priority make sex linked markers of DNA to test sex type in papaya then after DNA marker were widely used in papaya sex determination .On contrary in olden day papaya researchers and producers have long markers methods and techniques the first sex inked marker was found microsatellite containing the quandra nuclueotide repeats,(GATA) 4 [16-19] . Polymorphic
In this article, we have demonstrated that AEBP1 has a key role in modulation of in vivo adiposity. Detailed analysis of the transgenic mice indicates that AEBP1 may be a novel regulator of adiposity and energy balance in mammals. The present study clearly indicates that persistent overexpression of AEBP1 during adipocyte differentiation promotes HFD-induced obesity with increased in feed efficiency in female mice. Our data underscore a metabolic facet of AEBP1, which may operate as a novel effector of estrogen function linking energy metabolism. It has been well established that sex steroid hormones are involved in the regula- tion of metabolism, distribution, and accretion of adipose tissues. Homeostasis of adipose tissue requires proper amounts of estro- gens and androgens. In an aging population, as the levels of sex steroid hormones decrease, frequency of central obesity increases. Apparent positive effects on central obesity have been observed in older women by hormone replacement therapy and in aging men by testosterone therapy, with numerous side effects includ- ing bone loss and an increased risk for coronary heart disease, stroke, thromboembolic events, breast cancer, and prostate cancer (50). Our results suggest that AEBP1 may be a novel effector of estrogen action that is specific for adipose tissues and pathways related to lipid metabolism on the regulation of central obesity. Understanding the role AEBP1 plays in this regulation will lead to the eventual identification of potential molecular targets that may lead to novel methods of anti-obesity therapies.
The line along the catastrophe surface and across the catastro- in unmodified form) if segregation ratios are allowed phe curve corresponds to the section used to draw Figure 6. to differ between the sexes. This is because unlinked modifiers will sometimes favor enhanced segregation distortion if one of the heterozygous classes is the most fect drive in favor of one allele in one sex and against
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Genes with SDE were detected by two approaches from the NOISeq R package [31, 32] The first approach used the NOISeqBIO algorithm, which treats the sample population as biological replicates in which the com- puted variability within the population is considered as noise [31, 32]. We used this to compare gene reads per kilobase of transcript per million mapped reads (RPKM) expression values between women and men population samples from corresponding tissues after excluding un- informative genes, that is, genes that did not have at least an expression of 1 RPKM in any sample. A prob- ability cutoff of 0.95 was used to identify genes with sig- nificant differential expression, as this cutoff value is considered correct for multiple testing [31, 62]. The NOISeqBIO method provides effective statistics for de- termining differential expression between two popula- tions. However, this approach regards the population variability as noise and could exclude some genuinely sex-differentiated genes that have complex modes of ex- pression. For instance, genes activated during ovulation are expected to be expressed only in a few women (mainly in women <50 years old and on a few days each month ), while not being expressed in most women and in all men samples. The differential expression of such genes will be difficult to identify using a straightfor- ward population analysis. To detect at least some of these cases, we used an additional analysis approach that could identify the difference in such cases.
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