Sex Differences in Phonetic Processing: Speed of Identification of Alphabetical Sequences

Research on the sex difference in speed of matching strings of letters or digits has suggested that the difference is associated with the speed of the comparison and decision processes rather than with symbol recognition. In addition, the size of the difference is affected by whether the code used for the comparisons is figural or verbal. Given recent evidence on both the critical role of phonological processing in reading and sex differences in the lateralization of phonological processes in the brain, it was hypothesized that on a speeded task with high demands for phonological efficiency sex differences might be found even though no perceptual comparisons were required. In a study with 57 male and 60 female college students, the women were significantly faster in identifying alphabetical sequences and were more accurate than men. There were no significant sex differences on a perceptual matching condition. The results suggest that the verbal processes implicated in earlier work on sex differences in speed of symbol matching may be primarily due to sex differences in the efficiency of phonological processing.

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A critical role for central vasopressin in regulation of fever during bacterial infection

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1992.263.6.r1235 ◽

1992 ◽

Vol 263 (6) ◽

pp. R1235-R1240

Author(s):

R. A. Cridland ◽

N. W. Kasting

Keyword(s):

Body Temperature ◽

Arginine Vasopressin ◽

Continuous Measurement ◽

Critical Role ◽

Experimental Models ◽

Bacterial Endotoxins ◽

Chronic Infusion ◽

Live Bacteria ◽

The Brain

Previous investigations on the antipyretic properties of arginine vasopressin have used bacterial endotoxins or pyrogens to induce fever. Because these experimental models of fever fail to mimic all aspects of the responses to infection, we felt it was important to examine the role of endogenously released vasopressin as a neuromodulator in febrile thermoregulation during infection. Therefore the present study examines the effects of chronic infusion of a V1-receptor antagonist or saline (via osmotic minipumps into the ventral septal area of the brain) on a fever induced by injection of live bacteria. Telemetry was used for continuous measurement of body temperature in the awake unhandled rat. Animals infused with the V1-antagonist exhibited fevers that were greater in duration compared with those of saline-infused animals. These results support the hypothesis that vasopressin functions as an antipyretic agent or fever-reducing agent in brain. Importantly, they suggest that endogenously released vasopressin may play a role as a neuromodulator in natural fever.

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Epigenetic mechanisms in sexual differentiation of the brain and behaviour

Philosophical Transactions of the Royal Society B Biological Sciences ◽

10.1098/rstb.2015.0114 ◽

2016 ◽

Vol 371 (1688) ◽

pp. 20150114 ◽

Cited By ~ 34

Author(s):

Nancy G. Forger

Keyword(s):

Gene Expression ◽

Sex Differences ◽

Sexual Differentiation ◽

Wide Distribution ◽

Epigenetic Modifications ◽

Epigenetic Mechanism ◽

Epigenetic Mechanisms ◽

Genome Wide ◽

The Brain

Circumstantial evidence alone argues that the establishment and maintenance of sex differences in the brain depend on epigenetic modifications of chromatin structure. More direct evidence has recently been obtained from two types of studies: those manipulating a particular epigenetic mechanism, and those examining the genome-wide distribution of specific epigenetic marks. The manipulation of histone acetylation or DNA methylation disrupts the development of several neural sex differences in rodents. Taken together, however, the evidence suggests there is unlikely to be a simple formula for masculine or feminine development of the brain and behaviour; instead, underlying epigenetic mechanisms may vary by brain region or even by dependent variable within a region. Whole-genome studies related to sex differences in the brain have only very recently been reported, but suggest that males and females may use different combinations of epigenetic modifications to control gene expression, even in cases where gene expression does not differ between the sexes. Finally, recent findings are discussed that are likely to direct future studies on the role of epigenetic mechanisms in sexual differentiation of the brain and behaviour.

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Sex Differences and the Influence of Sex Hormones on Cognition through Adulthood and the Aging Process

Brain Sciences ◽

10.3390/brainsci8090163 ◽

2018 ◽

Vol 8 (9) ◽

pp. 163 ◽

Cited By ~ 17

Author(s):

Caroline Gurvich ◽

Kate Hoy ◽

Natalie Thomas ◽

Jayashri Kulkarni

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Sex Differences ◽

Cognitive Functioning ◽

Sex Hormones ◽

Reproductive Function ◽

Health And Disease ◽

And Function ◽

The Brain

Hormones of the hypothalamic-pituitary-gonadal (HPG) axis that regulate reproductive function have multiple effects on the development, maintenance and function of the brain. Sex differences in cognitive functioning have been reported in both health and disease, which may be partly attributed to sex hormones. The aim of the current paper was to provide a theoretical review of how sex hormones influence cognitive functioning across the lifespan as well as provide an overview of the literature on sex differences and the role of sex hormones in cognitive decline, specifically in relation to Alzheimer’s disease (AD). A summary of current hormone and sex-based interventions for enhancing cognitive functioning and/or reducing the risk of Alzheimer’s disease is also provided.

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Syk and Hrs Regulate TLR3-Mediated Antiviral Response in Murine Astrocytes

Oxidative Medicine and Cellular Longevity ◽

10.1155/2019/6927380 ◽

2019 ◽

Vol 2019 ◽

pp. 1-21 ◽

Cited By ~ 2

Author(s):

Matylda B. Mielcarska ◽

Magdalena Bossowska-Nowicka ◽

Karolina P. Gregorczyk-Zboroch ◽

Zbigniew Wyżewski ◽

Lidia Szulc-Dąbrowska ◽

...

Keyword(s):

Immune Responses ◽

Signaling Pathway ◽

Critical Role ◽

Antiviral Response ◽

Proteolytic Processing ◽

Viral Dsrna ◽

Kinase Substrate ◽

Tlr3 Signaling ◽

The Brain

Toll-like receptors (TLRs) sense the presence of pathogen-associated molecular patterns. Nevertheless, the mechanisms modulating TLR-triggered innate immune responses are not yet fully understood. Complex regulatory systems exist to appropriately direct immune responses against foreign or self-nucleic acids, and a critical role of hepatocyte growth factor-regulated tyrosine kinase substrate (HRS), endosomal sorting complex required for transportation-0 (ESCRT-0) subunit, has recently been implicated in the endolysosomal transportation of TLR7 and TLR9. We investigated the involvement of Syk, Hrs, and STAM in the regulation of the TLR3 signaling pathway in a murine astrocyte cell line C8-D1A following cell stimulation with a viral dsRNA mimetic. Our data uncover a relationship between TLR3 and ESCRT-0, point out Syk as dsRNA-activated kinase, and suggest the role for Syk in mediating TLR3 signaling in murine astrocytes. We show molecular events that occur shortly after dsRNA stimulation of astrocytes and result in Syk Tyr-342 phosphorylation. Further, TLR3 undergoes proteolytic processing; the resulting TLR3 N-terminal form interacts with Hrs. The knockdown of Syk and Hrs enhances TLR3-mediated antiviral response in the form of IFN-β, IL-6, and CXCL8 secretion. Understanding the role of Syk and Hrs in TLR3 immune responses is of high importance since activation and precise execution of the TLR3 signaling pathway in the brain seem to be particularly significant in mounting an effective antiviral defense. Infection of the brain with herpes simplex type 1 virus may increase the secretion of amyloid-β by neurons and astrocytes and be a causal factor in degenerative diseases such as Alzheimer’s disease. Errors in TLR3 signaling, especially related to the precise regulation of the receptor transportation and degradation, need careful observation as they may disclose foundations to identify novel or sustain known therapeutic targets.

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Biallelic variants in the small optic lobe calpain CAPN15 are associated with congenital eye anomalies, deafness and other neurodevelopmental deficits

Human Molecular Genetics ◽

10.1093/hmg/ddaa198 ◽

2020 ◽

Vol 29 (18) ◽

pp. 3054-3063

Author(s):

Congyao Zha ◽

Carole A Farah ◽

Richard J Holt ◽

Fabiola Ceroni ◽

Lama Al-Abdi ◽

...

Keyword(s):

Optic Lobe ◽

Critical Role ◽

Genetic Diagnosis ◽

Compound Heterozygous ◽

Clinical Genetic ◽

Eye Disorders ◽

Neurodevelopmental Deficits ◽

Independent Families ◽

The Brain

Abstract Microphthalmia, coloboma and cataract are part of a spectrum of developmental eye disorders in humans affecting ~12 per 100 000 live births. Currently, variants in over 100 genes are known to underlie these conditions. However, at least 40% of affected individuals remain without a clinical genetic diagnosis, suggesting variants in additional genes may be responsible. Calpain 15 (CAPN15) is an intracellular cysteine protease belonging to the non-classical small optic lobe (SOL) family of calpains, an important class of developmental proteins, as yet uncharacterized in vertebrates. We identified five individuals with microphthalmia and/or coloboma from four independent families carrying homozygous or compound heterozygous predicted damaging variants in CAPN15. Several individuals had additional phenotypes including growth deficits, developmental delay and hearing loss. We generated Capn15 knockout mice that exhibited similar severe developmental eye defects, including anophthalmia, microphthalmia and cataract, and diminished growth. We demonstrate widespread Capn15 expression throughout the brain and central nervous system, strongest during early development, and decreasing postnatally. Together, these findings demonstrate a critical role of CAPN15 in vertebrate developmental eye disorders, and may signify a new developmental pathway.

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Implementing the Team Approach in Higher Education

Industry and Higher Education ◽

10.5367/000000008785201775 ◽

2008 ◽

Vol 22 (4) ◽

pp. 245-251 ◽

Cited By ~ 1

Author(s):

Tracy M. Lara ◽

Aaron W. Hughey

Keyword(s):

Higher Education ◽

Needs Assessment ◽

Higher Education Administration ◽

Critical Role ◽

Education Administration ◽

Team Approach ◽

Academic Environment ◽

Team Efficacy ◽

The Difference

Many companies have implemented the team approach as a way to empower their employees in an effort to enhance productivity, quality and overall profitability. While application of the concept to higher education administration has been limited, colleges and universities could benefit from the team approach if implemented appropriately and conscientiously. The authors discuss some of the issues and concerns that are relevant to implementing the team approach in an academic environment. Suggestions for implementing teams in higher education are provided, including the difference between the team approach and traditional administration, the importance of a preliminary needs assessment, the development of an implementation plan, the critical role of leadership, dealing with issues of assessment and accountability, and the concept of team efficacy.

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Heterozygous variants in KCNC2 cause a broad spectrum of epilepsy phenotypes associated with characteristic functional alterations

10.1101/2021.05.21.21257099 ◽

2021 ◽

Author(s):

Niklas Schwarz ◽

Simone Seiffert ◽

Manuela Pendziwiat ◽

Annika Rademacher ◽

Tobias Bruenger ◽

...

Keyword(s):

Functional Analysis ◽

De Novo ◽

Critical Role ◽

Specific Response ◽

Loss Of Function ◽

Causative Gene ◽

Characteristic Functional ◽

Research Collaborations ◽

The Brain

Background KCNC2 encodes a member of the shaw-related voltage-gated potassium channel family (KV3.2), which are important for sustained high-frequency firing and optimized energy efficiency of action potentials in the brain. Methods Individuals with KCNC2 variants detected by exome sequencing were selected for clinical, further genetic and functional analysis. The cases were referred through clinical and research collaborations in our study. Four de novo variants were examined electrophysiologically in Xenopus laevis oocytes. Results We identified novel KCNC2 variants in 27 patients with various forms of epilepsy. Functional analysis demonstrated gain-of-function in severe and loss-of-function in milder phenotypes as the underlying pathomechanisms with specific response to valproic acid. Conclusion These findings implicate KCNC2 as a novel causative gene for epilepsy emphasizing the critical role of KV3.2 in the regulation of brain excitability with an interesting genotype-phenotype correlation and a potential concept for precision medicine.

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Role of astroglial Connexin 43 in pneumolysin cytotoxicity and during pneumococcal meningitis

PLoS Pathogens ◽

10.1371/journal.ppat.1009152 ◽

2020 ◽

Vol 16 (12) ◽

pp. e1009152

Author(s):

Chakir Bello ◽

Yasmine Smail ◽

Vincent Sainte-Rose ◽

Isabelle Podglajen ◽

Alice Gilbert ◽

...

Keyword(s):

Plasma Membrane ◽

Connexin 43 ◽

Critical Role ◽

Neurovascular Unit ◽

Brain Slices ◽

Host Cells ◽

Intermediate Filament Protein ◽

Young Infants ◽

The Brain

Streptococcus pneumoniae or pneumococcus (PN) is a major causative agent of bacterial meningitis with high mortality in young infants and elderly people worldwide. The mechanism underlying PN crossing of the blood brain barrier (BBB) and specifically, the role of non-endothelial cells of the neurovascular unit that control the BBB function, remains poorly understood. Here, we show that the astroglial connexin 43 (aCx43), a major gap junctional component expressed in astrocytes, plays a predominant role during PN meningitis. Following intravenous PN challenge, mice deficient for aCx43 developed milder symptoms and showed severely reduced bacterial counts in the brain. Immunofluorescence analysis of brain slices indicated that PN induces the aCx43–dependent destruction of the network of glial fibrillary acid protein (GFAP), an intermediate filament protein specifically expressed in astrocytes and up-regulated in response to brain injury. PN also induced nuclear shrinkage in astrocytes associated with the loss of BBB integrity, bacterial translocation across endothelial vessels and replication in the brain cortex. We found that aCx4-dependent astrocyte damages could be recapitulated using in vitro cultured cells upon challenge with wild-type PN but not with a ply mutant deficient for the pore-forming toxin pneumolysin (Ply). Consistently, we showed that purified Ply requires Cx43 to promote host cell plasma membrane permeabilization in a process involving the Cx43-dependent release of extracellular ATP and prolonged increase of cytosolic Ca2+ in host cells. These results point to a critical role for astrocytes during PN meningitis and suggest that the cytolytic activity of the major virulence factor Ply at concentrations relevant to bacterial infection requires co-opting of connexin plasma membrane channels.

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Glymphatics: A Transformative Development in Medical Neuroscience Relevant to Injuries in Military Central Nervous System

Military Medicine ◽

10.1093/milmed/usab344 ◽

2021 ◽

Author(s):

James Meyerhoff ◽

Nabarun Chakraborty ◽

Rasha Hammamieh

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Sleep Deprivation ◽

Brain Edema ◽

Critical Role ◽

Spatial Relationship ◽

Military Operations ◽

Glymphatic System ◽

The Brain

ABSTRACT Introduction The glia-operated glymphatic system, analogous to but separate from the lymphatics in the periphery, is unique to brain and retina, where it is very closely aligned with the arteriolar system. This intimate relationship leads to a “blood vessel like” distribution pattern of glymphatic vessels in the brain. The spatial relationship of glymphatics, including their essential component aquaporin-4 with vascular pericytes of brain arterioles is critical to functionality and is termed “polarization”. Materials and Methods We review the available literature on the factors affecting the resting state of glymphatics under normal conditions, including the important role of sleep in supporting normal glymphatic function (including waste removal) as well as the critical role of “polarization” under normal conditions. We then examine the effects of traumatic brain injury (TBI) or seizures on the glymphatic system and its state of “polarization”. Results Injury, such as TBI, can disrupt polarization resulting in “depolarization” leading to brain edema. Conclusion Damage to the glymphatic system might explain the brain edema so often seen following TBI or other insult. Moreover, similar damage should be expected in response to seizures, which can often be associated with chemical exposures as well as with TBI. Military operations, whether night operations or continuous operations, quite often impose limitations on sleep. As glymphatic function is sleep-dependent, sleep deprivation alone could compromise glymphatic function, as well, and might in addition, explain some of the well-known performance deficits associated with sleep deprivation. Possible effects of submarine and diving operations, chemical agents (including seizures), as well as high altitude exposure and other threats should be considered. In addition to the brain, the retina is also served and protected by the glymphatic system. Accordingly, the effect of military-related risks (e.g., exposure to laser or other threats) to retinal glymphatic function should also be considered. An intact glymphatic system is absolutely essential to support normal central nervous system functionality, including cognition. This effects a broad range of military threats on brain and retinal glymphatics should be explored. Possible preventive and therapeutic measures should be proposed and evaluated, as well.

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Cathelicidin Protects the Brain from Mitochondrial DNA Damage in Health, but not Following Septic Shock

10.21203/rs.3.rs-514325/v1 ◽

2021 ◽

Author(s):

Denise Frediani barbeiro ◽

Suely Kubo Ariga ◽

Hermes Vieira Barbeiro ◽

Nadja C Souza-Pinto ◽

Fabiano Pinheiro da Silva

Keyword(s):

Septic Shock ◽

Dna Damage ◽

Mitochondrial Dna ◽

Critical Role ◽

Innate Immune ◽

Experimental Sepsis ◽

Mitochondrial Dna Damage ◽

Innate Immune Signaling ◽

The Brain

Abstract Recent discoveries have demonstrated that mitochondria play a critical role in innate immune signaling. By the other hand, immune responses may lead to mitochondrial deregulation. Cathelicidins play a critical role in innate immunity, promoting poorly understood cellular responses that may enhance or inhibit several signaling pathways, depending on the health conditions and subjacent microenvironment.Here, we investigated the role of CRAMP, the murine cathelicidin, in healthy mice and following experimental sepsis. We found that sepsis induces significant mitochondrial DNA damage in the prefrontal cortex and that cathelicidin protects the brain from this kind of damage in healthy animals, but not following septic shock.

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