Role In Dimorphism Research Articles

Effects of Estradiol and Testosterone on the Expression of Growth‐related Genes in Female and Male Nile Tilapia, Oreochromis niloticus

AbstractNile tilapia exhibits strong sexual growth dimorphism. The potential role of sex steroid hormones in sexual growth dimorphism is not fully understood. We investigated the effects of estradiol (E2) and testosterone (T) on growth rate, plasma sex hormones, and expression of growth hormone (GH)‐insulin‐like growth factor (IGF) axis genes and muscle regulatory factor (MRF) genes in female and male Nile tilapia. The results revealed that serum concentrations of E2 and T were significantly higher after correlative injection (P < 0.05). Compared to male fish, female fish had lower growth rates. E2 increased growth performance in females with no significant effects on males, whereas T significantly increased growth performance in males, with no significant effects on females. In females, E2 significantly increased expression of ghr1, ghr2, igf1, and igf2, while T decreased igf2 and increased ghr1 and ghr2 expression. In males, T increased expression of igf1, igf2, ghr1, and ghr2, and E2 decreased expression of igf1, ghr1, and ghr2. Additionally, E2 and T enhanced the expression of MRF genes (myod1, myod2, myog, and myf5) in female and male fish, respectively. The results suggest that sex steroid hormones play a role in sexual growth dimorphism by regulating the expression of GH‐IGF axis and MRF genes.

MECHANISMS IN ENDOCRINOLOGY: The sexually dimorphic role of androgens in human metabolic disease.

Female androgen excess and male androgen deficiency manifest with an overlapping adverse metabolic phenotype, including abdominal obesity, insulin resistance, type 2 diabetes mellitus, non-alcoholic fatty liver disease and an increased risk of cardiovascular disease. Here, we review the impact of androgens on metabolic target tissues in an attempt to unravel the complex mechanistic links with metabolic dysfunction; we also evaluate clinical studies examining the associations between metabolic disease and disorders of androgen metabolism in men and women. We conceptualise that an equilibrium between androgen effects on adipose tissue and skeletal muscle underpins the metabolic phenotype observed in female androgen excess and male androgen deficiency. Androgens induce adipose tissue dysfunction, with effects on lipid metabolism, insulin resistance and fat mass expansion, while anabolic effects on skeletal muscle may confer metabolic benefits. We hypothesise that serum androgen concentrations observed in female androgen excess and male hypogonadism are metabolically disadvantageous, promoting adipose and liver lipid accumulation, central fat mass expansion and insulin resistance.

Prohibitin has sex dimorphic role in adipose and immune functions

The promoter of a gene that is selectively expressed in just a few cell types provides unique opportunities to study the pleiotropic function of a protein in two different cell types including the cell compartment specific function. This is not possible with a ubiquitous or a highly specific gene promoter. The adipocyte protein‐2 (aP2) is one such gene. It is primarily expressed in adipocytes, but also selectively in monocytic macrophages and dendritic cells among various immune cell types. Thus, the aP2 gene promoter provides an opportunity to simultaneously manipulate adipose and immune functions in a transgenic animal model.Prohibitin (PHB) is a pleiotropic protein with cell compartment specific functions such as mitochondria and the plasma membrane. New evidence suggests that PHB has roles in adipocyte and immune cells. To discern the cell compartment specific functions of PHB in adipocyte and immune cell, we developed two novel transgenic mice by expressing wild type PHB and a phospho mutant PHB (Y114F or m‐PHB) from the aP2 gene promoter, separately. Both transgenic mice develop obesity in a sex‐neutral manner suggesting that m‐PHB retains mitochondria‐related adipogenic function. However, both transgenic mice develop obesity‐related metabolic dysregulation in a male sex‐specific manner. Interestingly, the male PHB mice spontaneously developed T2D and liver cancer, whereas the male m‐PHB mice developed lymph node tumors, or T1D in a context‐dependent manner. This would imply that plasma membrane‐related phosphorylation of PHB at Tyr‐114 has a role in immune cell functions.Collectively, our data suggests that PHB has sex dimorphic roles in adipose and immune functions, which are mediated in a cell compartment specific manner. Also, we provide evidence that sex differences in adipose and immune functions contribute to sex differences in diabetes and cancer, which warrant further investigations.Support or Funding InformationSM is supported by funds from Natural Sciences and Engineering Research Council of Canada (NSERC) and Research Manitoba.

Sexual dimorphism of frailty and cognitive impairment: Potential underlying mechanisms (Review).

The aim of the present study was to assess systematically gender differences in susceptibility to frailty and cognitive performance decline, and the underlying mechanisms. A systematic assessment was performed of the identified reviews of cohort, mechanistic and epidemiological studies. The selection criteria of the present study included: i)Sexual dimorphism of frailty, ii)sexual dimorphism of subjective memory decline (impairment) and atrophy of hippocampus during early life, iii)sexual dimorphism of late‑onset Alzheimer's disease and iv)sexual dimorphism mechanisms underlying frailty and cognitive impairment. Males exhibit a susceptibility to poor memory performance and a severe atrophy of the hippocampus during early life and females demonstrate a higher prevalence for frailty and late‑life dementia. The different alterations within the hypothalamic‑pituitary‑gonadal/adrenal axis, particularly with regard to gonadal hormones, cortisol and dehydroepiandrosterone/sulfate‑bound dehydroepiandrosterone prior to and following andropause in males and menopause in females, serve important roles in sexual dimorphism of frailty and cognitive impairment. These endocrine changes may accelerate immunosenescence, weaken neuroprotective and neurotrophic effects, and promote muscle catabolism. The present study suggested that these age‑associated endocrine alterations interact with gender‑specific genetic and epigenetic factors, together with immunosenescence and iron accumulation. Environment factors, including psychological factors, are additional potential causes of the sexual dimorphism of frailty and cognitive impairment.

The Different Effects Of Endogenous And Exogenous Sex Hormones On Cerebrovascular Diseases

Background: A sexual dimorphism is seen in ischemic stroke. Women have lower stroke incidence than men until an advanced age, when the epidemiology of ischemic stroke shifts and incidence rises dramatically in women. This could indicate the role of sex hormones in pathogenesis of cerebrovascular diseases. This Review summarizes the sex differences related to stroke, and the effects of endogenous and exogenAous hormones on the cerebrovasculature of the male and female brain. 
 Methods: We conducted a vast review to analyze possible associations between exposure to endogenous and exogenous female and male steroid hormones and the risks of cerebrovascular diseases. This association is discussed in the context of the effects of sex hormone levels on the progression of atherosclerosis, the vascular tone, and various risk factors including patient's lipid profile, arterial blood pressure and diabetes. Their therapeutic potentials is also reviewed.
 Results: There is a debate on the role of androgens. A large array of data testifies in favor of a variety of neuroprotective androgen effects in men mostly, but in many cases in women as well. Testosterone supplementation in low to normal levels in hypogonadal men has mostly been shown to benefit the subjects receiving it, but administration in supraphysiological doses however, along with anabolic steroid abuse, seems to adversely affect both the lipid profile and insulin sensitivity in men. Its effects in women have yet to be researched in depth. Due to the lower stroke incidence observed in pre-menopausal women and robust preclinical evidence of neuroprotective and anti-inflammatory properties of estrogen, researchers have focused on the potential benefits of hormones to reduce ischemic brain injury. However, hormone therapy to postmenopausal females increases the risk and severity of ischemic stroke. Moreover, while estrogen treatment is neuroprotective in younger females, estrogen paradoxically increases infarct volume in acyclic females, which could be due to decreased availability of IGF-1, a neuroprotectant which decreases with advancing age and is down-regulated by estrogen treatment. A wealth of experimental evidence supports the neuroprotective properties of progesterone, and associated metabolites, following various types of central nervous system injury. In particular, for ischemic stroke, studies have also begun to reveal possible mechanisms of such neuroprotection.
 Conclusion: In conclusion, sex hormones have major roles in sex dimorphism in ischemic stroke. As the debate on the effects of sex hormones continues, understanding the minutie of the implication of them becomes increasingly important. An understanding of the effects of endogenous and exogenous estrogens on cerebral hemodynamics could guide research into explaining how sex hormones have paradoxical outcomes in ischemic events in men and women.

HO1 and Wnt expression is independently regulated in female mice brains following permanent ischemic brain injury

A gender difference in stroke is observed throughout epidemiologic studies, pathophysiology, treatment and outcomes. We investigated the neuroprotective role of hemeoxygenase (HO) enzyme, which catabolizes free heme to bilirubin, carbon monoxide and biliverdin in the female brain after permanent ischemia. We have previously reported in male mice that genetic deletion of HO1 exacerbates the brain damage after permanent ischemia, and the mechanism of neuroprotection is dependent on the HO1/Wnt pathway; however, the role of HO1/Wnt mediated neuroprotection in the female brain is yet to be investigated. We subjected ovary intact female mice, HO1−/− intact, HO1 inhibitor tin mesoporphyrin (SnMP) treated intact and/or ovariectomized female mice to permanent ischemia (pMCAO), and the animals were sacrificed after 7days. The SnMP treatment for 7days significantly reduced the HO1 enzyme activity as compared to that of vehicle treated group. Infarct volume analysis showed significantly lower infarct in intact, HO1−/− intact, and SnMP treated group as compared to the OVX group, suggesting the role of estrogen in neuroprotection. However, there were no differences in infarct volume observed between the intact, HO1−/− and SnMP treated group, suggesting a sexually dimorphic role of HO1 neuroprotection. Western blot analysis on intact and SnMP-treated groups subjected to pMCAO suggested no significant differences in Wnt expression. Together, these results suggest that HO1 neuroprotection is sexually dimorphic and Wnt expression is independently regulated in the female brain following permanent ischemia.

Possible sexually dimorphic role of miRNA and other sncRNA in ASD brain

BackgroundAutism spectrum disorder (ASD) is sexually dimorphic in brain structure, genetics, and behaviors. In studies of brain tissue, the age of the population is clearly a factor in interpreting study outcome, yet sex is rarely considered. To begin to address this issue, we extend our previously published microarray analyses to examine expression of small noncoding RNAs (sncRNAs), including microRNAs (miRNAs), in ASD and in the control temporal cortex in males and females. Predicted miRNA targets were identified as well as the pathways they overpopulate.FindingsAfter considering age, sexual dimorphism in ASD sncRNA expression persists in the temporal cortex and in the patterning that distinguishes regions. Among the sexually dimorphic miRNAs are miR-219 and miR-338, which promote oligodendrocyte differentiation, miR-125, implicated in neuronal differentiation, and miR-488, implicated in anxiety. Putative miRNA targets are significantly over-represented in immune and nervous system pathways in both sexes, consistent with previous mRNA studies. Even for common pathways, the specific target mRNAs are often sexually dimorphic. For example, both male and female target genes significantly populate the Axonal Guidance Signaling pathway, yet less than a third of the targets are common to both sexes.ConclusionsOur findings of sexual dimorphism in sncRNA levels underscore the importance of considering sex, in addition to age, when interpreting molecular findings on ASD brain.

Sexual Dimorphism in a Reciprocal Interaction of Ryanodine and IP3 Receptors in the Induction of Hyperalgesic Priming.

Hyperalgesic priming, a model of pain chronification in the rat, is mediated by ryanodine receptor-dependent calcium release. Although ryanodine induces priming in both sexes, females are 5 orders of magnitude more sensitive, by an estrogen receptor α (EsRα)-dependent mechanism. An inositol 1,4,5-triphosphate (IP3) receptor inhibitor prevented the induction of priming by ryanodine. For IP3 induced priming, females were also more sensitive. IP3-induced priming was prevented by pretreatment with inhibitors of the sarcoendoplasmic reticulum calcium ATPase and ryanodine receptor. Antisense to EsRα prevented the induction of priming by low-dose IP3 in females. The induction of priming by an EsRα agonist was ryanodine receptor-dependent and prevented by the IP3 antagonist. Thus, an EsRα-dependent bidirectional interaction between endoplasmic reticulum IP3 and ryanodine receptor-mediated calcium signaling is present in the induction of hyperalgesic priming, in females. In cultured male DRG neurons, IP3 (100 μm) potentiated depolarization-induced transients produced by extracellular application of high-potassium solution (20 mm, K20), in nociceptors incubated with β-estradiol. This potentiation of depolarization-induced calcium transients was blocked by the IP3 antagonist, and not observed in the absence of IP3 IP3 potentiation was also blocked by ryanodine receptor antagonist. The application of ryanodine (2 nm), instead of IP3, also potentiated K20-induced calcium transients in the presence of β-estradiol, in an IP3 receptor-dependent manner. Our results point to an EsRα-dependent, reciprocal interaction between IP3 and ryanodine receptors that contributes to sex differences in hyperalgesic priming.SIGNIFICANCE STATEMENT The present study demonstrates a mechanism that plays a role in the marked sexual dimorphism observed in a model of the transition to chronic pain, hyperalgesic priming. This mechanism involves a reciprocal interaction between the endoplasmic reticulum receptors, IP3 and ryanodine, in the induction of priming, regulated by estrogen receptor α in the nociceptor of female rats. The presence of this signaling pathway modulating the susceptibility of nociceptors to develop plasticity may contribute to our understanding of sex differences observed clinically in chronic pain syndromes.

Sex-dependent alteration of cardiac cytochrome P450 gene expression by doxorubicin in C57Bl/6 mice

BackgroundThere is inconclusive evidence about the role of sex as a risk factor for doxorubicin (DOX)-induced cardiotoxicity. Recent experimental studies have shown that adult female rats are protected against DOX-induced cardiotoxicity. However, the mechanisms of this sexual dimorphism are not fully elucidated. We have previously demonstrated that DOX alters the expression of several cytochrome P450 (CYP) enzymes in the hearts of male rats. Nevertheless, the sex-dependent effect of DOX on the expression of CYP enzymes is still not known. Therefore, in the present study, we determined the effect of acute DOX exposure on the expression of CYP genes in the hearts of both male and female C57Bl/6 mice.MethodsAcute DOX cardiotoxicity was induced by a single intraperitoneal injection of 20 mg/kg DOX in male and female adult C57Bl/6 mice. Cardiac function was assessed 5 days after DOX exposure by trans-thoracic echocardiography. Mice were euthanized 1 day or 6 days after DOX or saline injection. Thereafter, the hearts were harvested and weighed. Heart sections were evaluated for pathological lesions. Total RNA was extracted and expression of natriuretic peptides, inflammatory and apoptotic markers, and CYP genes was measured by real-time PCR.ResultsAdult female C57Bl/6 mice were protected from acute DOX-induced cardiotoxicity as they show milder pathological lesions, less inflammation, and faster recovery from DOX-induced apoptosis and DOX-mediated inhibition of beta-type natriuretic peptide. Acute DOX exposure altered the gene expression of multiple CYP genes in a sex-dependent manner. In 24 h, DOX exposure caused male-specific induction of Cyp1b1 and female-specific induction of Cyp2c29 and Cyp2e1.ConclusionsAcute DOX exposure causes sex-dependent alteration of cardiac CYP gene expression. Since cardiac CYP enzymes metabolize several endogenous compounds to biologically active metabolites, sex-dependent alteration of CYP genes may play a role in the sexual dimorphism of acute DOX-induced cardiotoxicity.

Do microglia play a role in sex differences in TBI?

Traumatic brain injury (TBI) is one of the leading causes of morbidity and mortality for both males and females and is, thus, a major focus of current study. Although the overall death rate of TBI for males is roughly three times higher than that for females, males have been disproportionately represented in clinical and preclinical studies. Gender differences are known to exist in many neurologic disorders, such as multiple sclerosis and stroke, and differences appear to exist in TBI. Furthermore, it is known that microglia have sexually dimorphic roles in CNS development and other neurologic conditions; however, most animal studies of microglia and TBI have focused on male subjects. Microglia are a current target of many preclinical and clinical therapeutic trials for TBI. Understanding the relationship among sex, sex hormones, and microglia is critical to truly understanding the pathophysiology of TBI. However, the evidence for sex differences in TBI centers mainly on sex hormones, and evidenced-based conclusions are often contradictory. In an attempt to review the current literature, it is apparent that sex differences likely exist, but the contradictory nature and magnitude of such differences in the existing literature does not allow definite conclusions to be drawn, except that more investigation of this issue is necessary. © 2016 Wiley Periodicals, Inc.

Genome-wide methylation analysis identified sexually dimorphic methylated regions in hybrid tilapia.

Sexual dimorphism is an interesting biological phenomenon. Previous studies showed that DNA methylation might play a role in sexual dimorphism. However, the overall picture of the genome-wide methylation landscape in sexually dimorphic species remains unclear. We analyzed the DNA methylation landscape and transcriptome in hybrid tilapia (Oreochromis spp.) using whole genome bisulfite sequencing (WGBS) and RNA-sequencing (RNA-seq). We found 4,757 sexually dimorphic differentially methylated regions (DMRs), with significant clusters of DMRs located on chromosomal regions associated with sex determination. CpG methylation in promoter regions was negatively correlated with the gene expression level. MAPK/ERK pathway was upregulated in male tilapia. We also inferred active cis-regulatory regions (ACRs) in skeletal muscle tissues from WGBS datasets, revealing sexually dimorphic cis-regulatory regions. These results suggest that DNA methylation contribute to sex-specific phenotypes and serve as resources for further investigation to analyze the functions of these regions and their contributions towards sexual dimorphisms.

Sexual dimorphism in the glucose homeostasis phenotype of the Aromatase Knockout (ArKO) mice

We investigated the effects of estrogens on glucose homeostasis using the Aromatase Knockout (ArKO) mouse, which is unable to convert androgens into estrogens. The ArKO mouse is a model of total estrogen ablation which develops symptoms of metabolic syndrome.To determine the development and progression of whole body state of insulin resistance of ArKO mice, comprehensive whole body tolerance tests were performed on WT, ArKO and estrogen administrated mice at 3 and 12 months of age. The absence of estrogens in the male ArKO mice leads to hepatic insulin resistance, glucose and pyruvate intolerance from 3 to 12 months with consistent improvement upon estrogen treatment. Estrogen absence in the female ArKO mice leads to glucose intolerance without pyruvate intolerance or insulin resistance. The replacement of estrogens in the female WT and ArKO mice exhibited both insulin sensitizing and resistance effects depending on age and dosage.In conclusion, this study presents information on the sexually dimorphic roles of estrogens on glucose homeostasis regulation.

Maternal flaxseed oil intake during lactation changes body fat, inflammatory markers and glucose homeostasis in the adult progeny: role of gender dimorphism

We evaluated maternal flaxseed oil intake during lactation on body composition, lipid profile, glucose homeostasis and adipose tissue inflammation in male and female progeny at adulthood. Lactating rats were divided into the following: control 7% soybean oil (C), hyper 19% soybean oil (HS) and hyper 17% flaxseed oil+2% soybean oil (HF). Weaned pups received a standard diet. Offspring were killed in PN180. Male HF presented higher visceral adipose tissue (VAT) and triacylglycerol, and female HF showed insulin resistance. Both male and female HF had hyperleptinemia, and only male HF had hyperprolactinemia. In VAT, male HF presented lower PPAR-γ expressions and higher TNF-α, IL-6, IL-1β and IL-10 expressions; in subcutaneous adipose tissue (SAT), they presented lower PPAR-γ and TNF-α expressions. Female HF presented higher leptin, as well as lower adiponectin, TNF-α, IL-6 and IL-1β expressions in VAT and lower TNF-α in SAT. Flaxseed oil during lactation leads to gender-specific effects with more adiposity and dyslipidemia in male and insulin resistance in female. Higher prolactin and inflammatory cytokines in male could play a role in these gender differences. We suggest that the use of flaxseed oil during lactation increases metabolic syndrome risk in the adult progeny.

Sa1681 Ret Receptor Tyrosine Kinase Plays a Sexually Dimorphic Role in the Regulation of Gastrointestinal Motility and Is Expressed by Distinct Subsets of Enteric Neurons Important for Peristalsis

Sa1681 Ret Receptor Tyrosine Kinase Plays a Sexually Dimorphic Role in the Regulation of Gastrointestinal Motility and Is Expressed by Distinct Subsets of Enteric Neurons Important for Peristalsis

Testosterone reduces functional connectivity during the ‘Reading the Mind in the Eyes’ Test

Women on average outperform men in cognitive-empathic abilities, such as the capacity to infer motives from the bodily cues of others, which is vital for effective social interaction. The steroid hormone testosterone is thought to play a role in this sexual dimorphism. Strikingly, a previous study shows that a single administration of testosterone in women impairs performance on the ‘Reading the Mind in Eyes’ Test (RMET), a task in which emotions have to be inferred from the eye-region of a face. This effect was mediated by the 2D:4D ratio, the ratio between the length of the index and ring finger, a proxy for fetal testosterone. Research in typical individuals, in individuals with autism spectrum conditions (ASC), and in individuals with brain lesions has established that performance on the RMET depends on the left inferior frontal gyrus (IFG). Using functional magnetic resonance imaging (fMRI), we found that a single administration of testosterone in 16 young women significantly altered connectivity of the left IFG with the anterior cingulate cortex (ACC) and the supplementary motor area (SMA) during RMET performance, independent of 2D:4D ratio. This IFG-ACC-SMA network underlies the integration and selection of sensory information, and for action preparation during cognitive empathic behavior. Our findings thus reveal a neural mechanism by which testosterone can impair emotion-recognition ability, and may link to the symptomatology of ASC, in which the same neural network is implicated.

Editorial: Exploring Gender and Sex Differences in Behavioral Dyscontrol: From Drug Addiction to Impulse Control Disorders.

Editorial: Exploring Gender and Sex Differences in Behavioral Dyscontrol: From Drug Addiction to Impulse Control Disorders.

Effect of linoleic acid on reproduction and yeast–mycelium dimorphism in the Dutch elm disease pathogens

Elm populations from North America and Europe were devastated by Dutch elm disease (DED), which is a vascular disease caused by fungi from the genus Ophiostoma (Ascomycota). These pathogens feature a yeast–mycelium dimorphism that may be related to virulence by facilitating colonization of the host xylem. Cyclooxygenases (COX) have been proposed to modulate yeast–mycelium dimorphism of DED fungi, and homologs of cox genes have been found in the nuclear genome of O. novo-ulmi subsp. novo-ulmi. Linoleic acid, a substrate for COX, was reported to stimulate the formation of asexual and sexual reproduction structures in DED strains grown on complex media. We hypothesized that linoleic acid also induced mycelium production in liquid shake culture conditions. Linoleic acid was found to enhance the production of reproductive structures in sexual crosses conducted on a complex medium (elm sapwood agar), but was not sufficient for these structures to form on a minimal medium. In liquid shake cultures grown in a minimal medium, the addition of linoleic acid stimulated mycelial formation. Our results suggest that linoleic acid plays a role in reproduction and dimorphism in the DED pathogens.

Prion Diseases in Animals and Zoonotic Potential.

Dietary exposure to Bovine Spongiform Encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt-Jakob disease (vCJD) in humans. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of transmissible spongiform encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants, there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt-Jakob disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modelling of the "species barrier," the biological phenomenon that limits TSE agents' propagation from one species to another. In the past decade, mice genetically engineered to express normal forms of the human prion protein have proven to be essential in studying human prions pathogenesis and modelling the capacity of TSEs to cross the human species barrier. To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents. These transmission experiments confirm the ability of BSE prions to propagate in 129M-HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goats to a greater degree than the BSE agent in cattle, and that these agents can convey molecular properties and be neuropathologically indistinguishable from vCJD. However, homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species, suggesting a higher transmission barrier for 129V-PrP variant. Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

Foramen magnum as a tool for sexual dimorphism: A cone beam computed tomography study.

(1) To evaluate dimensions of the foramen magnum (FM) among males and females and to establish its role in sexual dimorphism using cone beam computed tomography (CBCT). (2) To evaluate sagittal diameter, transverse diameter, area, and circumference of FM among males and females. Two hundred and eighty CBCT scans (140 males and 140 females; age range, 20-80 years) were selected for this study. The sagittal diameter, transverse diameter, area, and circumference of FM were measured, and data were subjected to discriminant analysis for the evaluation of sexual dimorphism. The area of FM was the best discriminant parameter which is used to study the sexual dimorphism with an overall accuracy of 72%. It can be concluded that the reconstructed CBCT image provides valuable measurements for the FM and could be used for sexing even when other methods are inconclusive.

Role of Heat-Shock Proteins in Cellular Function and in the Biology of Fungi.

Stress (biotic or abiotic) is an unfavourable condition for an organism including fungus. To overcome stress, organism expresses heat-shock proteins (Hsps) or chaperons to perform biological function. Hsps are involved in various routine biological processes such as transcription, translation and posttranslational modifications, protein folding, and aggregation and disaggregation of proteins. Thus, it is important to understand holistic role of Hsps in response to stress and other biological conditions in fungi. Hsp104, Hsp70, and Hsp40 are found predominant in replication and Hsp90 is found in transcriptional and posttranscriptional process. Hsp90 and Hsp70 in combination or alone play a major role in morphogenesis and dimorphism. Heat stress in fungi expresses Hsp60, Hsp90, Hsp104, Hsp30, and Hsp10 proteins, whereas expression of Hsp12 protein was observed in response to cold stress. Hsp30, Hsp70, and Hsp90 proteins showed expression in response to pH stress. Osmotic stress is controlled by small heat-shock proteins and Hsp60. Expression of Hsp104 is observed under high pressure conditions. Out of these heat-shock proteins, Hsp90 has been predicted as a potential antifungal target due to its role in morphogenesis. Thus, current review focuses on role of Hsps in fungi during morphogenesis and various stress conditions (temperature, pH, and osmotic pressure) and in antifungal drug tolerance.