8. Coming-to-Head, Returning-to-Womb: (E)Soteric Gnosis and Overcoming Gender Dimorphism

In the present study, we have investigated gender differences in rat liver mitochondrial oxidative metabolism. Total mitochondrial population (M) as well as the heavy (M1), medium (M3), and light (M8) mitochondrial fractions obtained by means of differential centrifugation steps at 1,000, 3,000, and 8,000 g, respectively, were isolated. Electron microscopic analysis was performed and mitochondrial protein content and cardiolipin levels, mitochondrial O2 flux, ATP synthase activity, mitochondrial membrane potential, and mitochondrial transcription factor A (TFAM) protein levels were measured in each sample. Our results indicate that mitochondria from females have higher protein content and higher cardiolipin levels, greater respiratory and phosphorylative capacities, and more-energized mitochondria in respiratory state 3. Moreover, protein levels of TFAM were four times greater in females than in males. Gender differences in the aforementioned parameters were more patent in the isolated heavy M1 and M3 mitochondrial fractions. The present study demonstrates that gender-related differences in liver mitochondrial function are due mainly to a higher capacity and efficiency of substrate oxidation, likely related to greater mitochondrial machinery in females than in males, which is in accord with greater mitochondrial differentiation in females.

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Arch Widths in Class II-2 Adults Compared to Adults with Class II-1 and Normal Occlusion

The Angle Orthodontist ◽

10.2319/062305-209 ◽

2007 ◽

Vol 77 (5) ◽

pp. 837-844 ◽

Cited By ~ 14

Author(s):

Joel Huth ◽

Robert Newton Staley ◽

Richard Jacobs ◽

Harold Bigelow ◽

Jane Jakobsen

Keyword(s):

Class Ii ◽

White Americans ◽

Gender Dimorphism ◽

Arch Width ◽

Normal Occlusion ◽

Division 1 ◽

History Of ◽

Division 2 ◽

Male Subjects ◽

Female Subjects

Abstract Objective: To compare (1) arch widths in adults with Class II division 2 (II-2), Class II division 1 (II-1), and Class I normal occlusions, (2) genders, (3) gender dimorphism, (4) differences between maxillary and mandibular arch widths, and to (5) develop adult norms for arch widths. Materials and Methods: Subjects were white Americans with no history of orthodontic treatment. Arch width dimensions measured were: intercanine, intermolar, and molar alveolar in both arches. Analysis of variance (ANOVA) and Duncan's test were used to compare groups. Results: Comparison of pooled genders showed the II-2 group had maxillary arch widths significantly smaller than the normal occlusions and significantly larger than the II-1 group. All groups had similar mandibular intercanine and alveolar widths. The II-2 and II-1 groups had similar mandibular intermolar widths, both significantly smaller than normal occlusions. The II-2 group had a maxillary/mandibular intermolar difference significantly smaller than the normal occlusions, and significantly less negative than the II-1 group. Gender comparisons in two of six widths showed normal and II-2 male subjects were similar, and in six of six widths normal and II-2 female subjects were similar; in five of six widths II-2 and II-1 male and female subjects were similar. Gender dimorphism occurred in five of six widths in normal occlusions, four of six widths in II-2, and one of six widths in II-1. Conclusions: Arch width dimensions of II-2 subjects were intermediate between normal and II-1 occlusions. In both Class II malocclusions, the process that narrows arch widths was more pronounced in male than in female subjects.

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The contribution of epigenetics to the pathogenesis and gender dimorphism of systemic sclerosis: a comprehensive overview

Therapeutic Advances in Musculoskeletal Disease ◽

10.1177/1759720x20918456 ◽

2020 ◽

Vol 12 ◽

pp. 1759720X2091845 ◽

Cited By ~ 1

Author(s):

Bianca Saveria Fioretto ◽

Irene Rosa ◽

Eloisa Romano ◽

Yukai Wang ◽

Serena Guiducci ◽

...

Keyword(s):

Systemic Sclerosis ◽

X Chromosome ◽

Clinical Manifestations ◽

Connective Tissue Disorder ◽

Epigenetic Modifications ◽

Unknown Etiology ◽

Comprehensive Overview ◽

Gender Dimorphism ◽

Immune Related Genes ◽

The Right

Systemic sclerosis (SSc) is a life-threatening connective tissue disorder of unknown etiology characterized by widespread vascular injury and dysfunction, impaired angiogenesis, immune dysregulation and progressive fibrosis of the skin and internal organs. Over the past few years, a new trend of investigations is increasingly reporting aberrant epigenetic modifications in genes related to the pathogenesis of SSc, suggesting that, besides genetics, epigenetics may play a pivotal role in disease development and clinical manifestations. Like many other autoimmune diseases, SSc presents a striking female predominance, and even if the reason for this gender imbalance has yet to be completely understood, it appears that the X chromosome, which contains many gender and immune-related genes, could play a role in such gender-biased prevalence. Besides a short summary of the genetic background of SSc, in this review we provide a comprehensive overview of the most recent insights into the epigenetic modifications which underlie the pathophysiology of SSc. A particular focus is given to genetic variations in genes located on the X chromosome as well as to the main X-linked epigenetic modifications that can influence SSc susceptibility and clinical phenotype. On the basis of the most recent advances, there is realistic hope that integrating epigenetic data with genomic, transcriptomic, proteomic and metabolomic analyses may provide in the future a better picture of their functional implications in SSc, paving the right way for a better understanding of disease pathogenesis and the development of innovative therapeutic approaches.

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Gender dimorphism of indicators of heart rate, central hemodynamics and physical performance of runners on a distance of 100–200 meters

Current issues in pharmacy and medicine science and practice ◽

10.14739/2409-2932.2016.2.71131 ◽

2016 ◽

Vol 0 (2) ◽

Author(s):

E. L. Mikhalyuk ◽

M. V. Didenko ◽

S. N. Malakhova

Keyword(s):

Heart Rate ◽

Physical Performance ◽

Central Hemodynamics ◽

Gender Dimorphism

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Treadmill Exercise-Dependent Tumor Growth Retardation in T-Cell Lymphoma-Bearing Host Displays Gender Dimorphism

Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics ◽

10.3727/096504010x12629634366142 ◽

2009 ◽

Vol 18 (7) ◽

pp. 293-304 ◽

Cited By ~ 9

Author(s):

Vinod Kumar Verma ◽

Vivek Singh ◽

Mahendra Pal Singh ◽

Sukh Mahendra Singh

Keyword(s):

T Cell ◽

Tumor Growth ◽

Growth Retardation ◽

Treadmill Exercise ◽

Cell Lymphoma ◽

T Cell Lymphoma ◽

Gender Dimorphism

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Abstract 17462: Relevance of Regulatory T Cells to Gender Dimorphism in Pulmonary Hypertension

Circulation ◽

10.1161/circ.132.suppl_3.17462 ◽

2015 ◽

Vol 132 (suppl_3) ◽

Author(s):

Rasa Tamosiuniene ◽

Linh Nguyen ◽

Ayala Luria ◽

Joshua Sante ◽

Toshie Saito ◽

...

Keyword(s):

T Cell ◽

Vascular Wall ◽

Reciprocal Relationship ◽

Female Rats ◽

Gender Dimorphism ◽

Control Male ◽

Control Female ◽

Male And Female Rats ◽

Endogenous Estrogen

Idiopathic Pulmonary Arterial Hypertension (IPAH) is a disease with female predominance. A growing body of evidence shows reciprocal relationship between sex steroids and the immune system. The aim of the present study was to determine whether the absence of Tregs with the presence of endogenous estrogen mediate the development of PH in a gender-specific manner and if protective signaling pathways of Tregs prevent gender dimorphism of PH susceptibility in T cell deficient animal model of PH. Methods and Results: in two utilized models of PH inbred Wag T cell deficient athymic (AT) nude male and female rats were given s/c SU5416 in normoxia or treated with chronic hypoxia (CH) for 21d. In IR experiments, AT rats received purified CD4+CD25+hi/Tregs. We also tested the effect of murine/human Tregs or CD4+CD25- on primary rat lung, cardiac and human lung microvascular ECs (RLMECs, HLMECs, RCMECs) with set-up of cocultures. In both PH models treatment resulted in development of PH with significantly higher RVSP and particular significantly pronounced RVH in female than in male in both SU5416 and CH groups (Fulton index: 0.41±0.01vs.0.33±0.02 and 0.52±0.03vs.0.37±0.01, p< 0.05). However, circulating estrogen levels were found to be significantly elevated in female than in male in all animal groups. For both female and male AT animals IR of Tregs prevented PH with RV remodeling, as well as decreased perivascular fibrosis and increased estrogen receptor (ER)β expression in lung and RV vascular wall. In vitro studies on coculture of Tregs with RLMECs and RCMECs resulted in an upregulation of IL-10, HO-1, PDL1, ERα, ERβ, activation of pAKT pathway, and endothelial nitric oxide synthase (eNOS), which was abrogated with ER antagonist ICI182,780. In addition, compared with control male AT rats, control female animals had increased expression of HO1, HO2 enzymes in lung and RV vascular wall endothelial/Reca+ cells as well as increased capillary density in RV. Thus, differential HO expression between the genders might account for the PH susceptibility. Conclusions: Our data suggest that Tregs signaling is required as a major mechanism with possible mutual interaction of endogenous estrogen to prevent endothelial injury related gender dimorphism for the development of PH.

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