rudyvdbrink/CitationDatabase huggingface dataset:
A longitudinal analysis of women's salivary testosterone and intrasexual competitiveness.
Psychoneuroendocrinology, 2016

Research on within-subject changes in women's intrasexual competitiveness has generally focused on possible relationships between women's intrasexual competitiveness and estimates of their fertility. While this approach is useful for testing hypotheses about the adaptive function of changes in women's intrasexual competitiveness, it offers little insight into the proximate mechanisms through which such changes might occur. To investigate this issue, we carried out a longitudinal study of the hormonal correlates of changes in intrasexual competitiveness in a large sample of heterosexual women (N=136). Each woman provided saliva samples and completed an intrasexual competitiveness questionnaire in five weekly test sessions. Multilevel modeling of these data revealed a significant, positive within-subject effect of testosterone on intrasexual competitiveness, indicating that women reported greater intrasexual competitiveness when testosterone was high. By contrast, there were no significant effects of estradiol, progesterone, estradiol-to-progesterone ratio, or cortisol and no significant effects of any hormones on reported relationship jealousy. This is the first study to demonstrate correlated changes in measured testosterone levels and women's reported intrasexual competitiveness, implicating testosterone in the regulation of women's intrasexual competitiveness.
Emotion potentiated startle in fragile X syndrome.
Journal of autism and developmental disorders, 2014

Social avoidance and anxiety are prevalent in fragile X syndrome (FXS) and are potentially mediated by the amygdala, a brain region critical for social behavior. Unfortunately, functional brain resonance imaging investigation of the amygdala in FXS is limited by the difficulties experienced by intellectually impaired and anxious participants. We investigated the relationship between social avoidance and emotion-potentiated startle, a probe of amygdala activation, in children and adolescents with FXS, developmental disability without FXS (DD), and typical development. Individuals with FXS or DD demonstrated significantly reduced potentiation to fearful faces than a typically developing control group (p < .05). However, among individuals with FXS, social avoidance correlated positively with fearful-face potentiation (p < .05). This suggests that general intellectual disability blunts amygdalar response, but differential amygdala responsiveness to social stimuli contributes to phenotypic variability among individuals with FXS.
The Neuroscience of Goals and Behavior Change.
Consulting psychology journal, 2018

The ways that people set, pursue, and eventually succeed or fail in accomplishing their goals are central issues for consulting psychology. Goals and behavior change have long been the subject of empirical investigation in psychology, and have been adopted with enthusiasm by the cognitive and social neurosciences in the last few decades. Though relatively new, neuroscientific discoveries have substantially furthered the scientific understanding of goals and behavior change. This article reviews the emerging brain science on goals and behavior change, with particular emphasis on its relevance to consulting psychology. I begin by articulating a framework that parses behavior change into two dimensions, one motivational (the
The Peculiar Pattern of Type IV Collagen Deposition in Epiretinal Membranes.
The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 2020

Idiopathic epiretinal membranes are sheets of tissue that develop in the vitreoretinal interface. They are formed by cells and extracellular matrix, and they are considered the expression of a fibrotic disorder of the eye. Confocal and immunoelectron microscopy of the extracellular matrix of excised membranes, revealed high contents of type IV collagen. It was distributed within epiretinal membranes in basement membrane-like structures associated with cells and in interstitial deposits. In both cases, type IV collagen was always associated with type I collagen. Col IV was also coupled with Col VI and laminin. At high magnification, type IV collagen immunolabelling was associated with interstitial deposits and showed a reticular appearance due to the intersection of beaded microfilaments. The microfilaments are about 12 nm in diameter with interbead distance of 30-40 nm. Cells of the epiretinal membranes showed intracellular lysosome-like bodies heavily labeled for type IV collagen suggesting an active role in membrane remodeling. Hence, type IV collagen is not necessarily always associated with basement membranes; the molecular interactions that it may develop when not incorporated in basement membranes are still unknown. It is conceivable, however, that they might have implications in the progression of epiretinal membranes and other fibrotic disorders.
Comparing various protocols of human and bovine ovarian tissue decellularization to prepare extracellular matrix-alginate scaffold for better follicle development in vitro.
BMC biotechnology, 2021

Nowadays, the number of cancer survivors is significantly increasing as a result of efficient chemo/radio therapeutic treatments. Female cancer survivors may suffer from decreased fertility. In this regard, different fertility preservation techniques were developed. Artificial ovary is one of these methods suggested by several scientific groups. Decellularized ovarian cortex has been introduced as a scaffold in the field of human fertility preservation. This study was carried out to compare decellularization of the ovarian scaffold by various protocols and evaluate the follicle survival in extracellular matrix (ECM)-alginate scaffold.
Dim light at night disrupts molecular circadian rhythms and increases body weight.
Journal of biological rhythms, 2013

With the exception of high latitudes, life has evolved under bright days and dark nights. Most organisms have developed endogenously driven circadian rhythms that are synchronized to this daily light/dark cycle. In recent years, humans have shifted away from the naturally occurring solar light cycle in favor of artificial and sometimes irregular light schedules produced by electric lighting. Exposure to unnatural light cycles is increasingly associated with obesity and metabolic syndrome; however, the means by which environmental lighting alters metabolism are poorly understood. Thus, we exposed mice to dim light at night and investigated changes in the circadian system and metabolism. Here we report that exposure to ecologically relevant levels of dim (5 lux) light at night altered core circadian clock rhythms in the hypothalamus at both the gene and protein level. Circadian rhythms in clock expression persisted during light at night; however, the amplitude of Per1 and Per2 rhythms was attenuated in the hypothalamus. Circadian oscillations were also altered in peripheral tissues critical for metabolic regulation. Exposure to dimly illuminated, as compared to dark, nights decreased the rhythmic expression in all but one of the core circadian clock genes assessed in the liver. Additionally, mice exposed to dim light at night attenuated Rev-Erb expression in the liver and adipose tissue. Changes in the circadian clock were associated with temporal alterations in feeding behavior and increased weight gain. These results are significant because they provide evidence that mild changes in environmental lighting can alter circadian and metabolic function. Detailed analysis of temporal changes induced by nighttime light exposure may provide insight into the onset and progression of obesity and metabolic syndrome, as well as other disorders involving sleep and circadian rhythm disruption.
A novel amyotrophic lateral sclerosis mutation in OPTN induces ER stress and Golgi fragmentation in vitro.
Amyotrophic lateral sclerosis & frontotemporal degeneration, 2017

Mutations in the optineurin gene (OPTN) have been identified in a small proportion (<1%) of sporadic and familial ALS cases, and the exact role of optineurin in the pathogenesis of ALS remains unclear. To further examine the role of OPTN in ALS, we sought to identify novel ALS variants in OPTN and examine their potential for pathogenicity in vitro. Whole exome sequence data from 74 familial ALS cases were analysed for the presence of novel OPTN mutations. Pathogenicity was assessed by analysing effects on Golgi fragmentation, endoplasmic reticulum (ER) stress-linked CHOP activation, and cellular localization of optineurin in motor neuron-like NSC-34 cells expressing mutant optineurin. We identified a novel heterozygous missense mutation in OPTN (c.883G > T, p.Val295Phe) in a single familial ALS case. This mutation induced recognized cellular features of ALS pathogenesis including Golgi fragmentation and ER stress in NSC-34 cells. In conclusion, the identification of a novel OPTN mutation in an Australian ALS family, and its capacity to induce ALS-like pathological features in vitro, further strengthens evidence for the role of optineurin in the pathogenesis of ALS.
Implicit learning of between-group intervals in auditory temporal structures.
Attention, perception & psychophysics, 2016

Implicit learning of temporal structure has primarily been reported when events within a sequence (e.g., visual-spatial locations, tones) are systematically ordered and correlated with the temporal structure. An auditory serial reaction time task was used to investigate implicit learning of temporal intervals between pseudorandomly ordered syllables. Over exposure, participants identified syllables presented in sequences with weakly metrical temporal structures. In a test block, the temporal structure differed from exposure only in the duration of the interonset intervals (IOIs) between groups. It was hypothesized that reaction time (RT) to syllables following between-group IOIs would decrease with exposure and increase at test. In Experiments 1 and 2, the sequences presented over exposure and test were counterbalanced across participants (Pattern 1 and Pattern 2 conditions). An RT increase at test to syllables following between-group IOIs was only evident in the condition that presented an exposure structure with a slightly stronger meter (Pattern 1 condition). The Pattern 1 condition also elicited a global expectancy effect: Test block RT slowed to earlier-than-expected syllables (i.e., syllables shifted to an earlier beat) but not to later-than-expected syllables. Learning of between-group IOIs and the global expectancy effect extended to the Pattern 2 condition when meter was strengthened with an external pulse (Experiment 2). Experiment 3 further demonstrated implicit learning of a new weakly metrical structure with only earlier-than-expected violations at test. Overall findings demonstrate learning of weakly metrical rhythms without correlated event structures (i.e., sequential syllable orders). They further suggest the presence of a global expectancy effect mediated by metrical strength.
Bilateral and asymmetrical contributions of passive and active ankle plantar flexors stiffness to spasticity in humans with spinal cord injury.
Journal of neurophysiology, 2020

Spasticity is one of the most common symptoms present in humans with spinal cord injury (SCI); however, its clinical assessment remains underdeveloped. The purpose of the study was to examine the contribution of passive muscle stiffness and active spinal reflex mechanisms to clinical outcomes of spasticity after SCI. It is important that passive and active contributions to increased muscle stiffness are distinguished to make appropriate decisions about antispastic treatments and to monitor its effectiveness. To address this question, we combined biomechanical and electrophysiological assessments of ankle plantarflexor muscles bilaterally in individuals with and without chronic SCI. Spasticity was assessed using the Modified Ashworth Scale (MAS) and a self-reported questionnaire. We performed slow and fast dorsiflexion stretches of the ankle joint to measure passive muscle stiffness and reflex-induced torque using a dynamometer and the soleus H reflex using electrical stimulation over the posterior tibial nerve. All SCI participants reported the presence of spasticity. While 96% of them reported higher spasticity on one side compared with the other, the MAS detected differences across sides in only 25% of the them. Passive muscle stiffness and the reflex-induced torque were larger in SCI compared with controls more on one side compared with the other. The soleus stretch reflex, but not the H reflex, was larger in SCI compared with controls and showed differences across sides, with a larger reflex in the side showing a higher reflex-induced torque. MAS scores were not correlated with biomechanical and electrophysiological outcomes. These findings provide evidence for bilateral and asymmetric contributions of passive and active ankle plantar flexors stiffness to spasticity in humans with chronic SCI and highlight a poor agreement between a self-reported questionnaire and the MAS for detecting asymmetries in spasticity across sides.
Involvement of adenosine monophosphate activated kinase in interleukin-6 regulation of steroidogenic acute regulatory protein and cholesterol side chain cleavage enzyme in the bovine zona fasciculata and zona reticularis.
Steroids, 2018

In bovine adrenal zona fasciculata (ZF) and NCI-H295R cells, interleukin-6 (IL-6) increases cortisol release, increases expression of steroidogenic acute regulatory protein (StAR), cholesterol side chain cleavage enzyme (P450scc), and steroidogenic factor 1 (SF-1) (increases steroidogenic proteins), and decreases the expression of adrenal hypoplasia congenita-like protein (DAX-1) (inhibits steroidogenic proteins). In contrast, IL-6 decreases bovine adrenal zona reticularis (ZR) androgen release, StAR, P450scc, and SF-1 expression, and increases DAX-1 expression. Adenosine monophosphate (AMP) activated kinase (AMPK) regulates steroidogenesis, but its role in IL-6 regulation of adrenal steroidogenesis is unknown. In the present study, an AMPK activator (AICAR) increased (P < 0.01) NCI-H295R StAR promoter activity, StAR and P450scc expression, and the phosphorylation of AMPK (PAMPK) and acetyl-CoA carboxylase (PACC) (indexes of AMPK activity). In ZR (decreased StAR, P450scc, SF-1, increased DAX-1) (P < 0.01) and ZF tissues (increased StAR, P450scc, SF-1, decreased DAX-1) (P < 0.01), AICAR modified StAR, P450scc, SF-1 and DAX-1 mRNAs/proteins similar to the effects of IL-6. The activity (increased PAMPK and PACC) (P < 0.01) of AMPK in the ZF and ZR was increased by AICAR and IL-6. In support of an AMPK role in IL-6 ZF and ZR effects, the AMPK inhibitor compound C blocked (P < 0.01) the effects of IL-6 on the expression of StAR, P450scc, SF-1, and DAX-1. Therefore, IL-6 modification of the expression of StAR and P450scc in the ZF and ZR may involve activation of AMPK and these changes may be related to changes in the expression of SF-1 and DAX-1.
VEGF plasma level variations in duloxetine-treated patients with major depression.
Journal of affective disorders, 2013

The vascular endothelial growth factor (VEGF) signaling, which modulates angiogenesis and neurogenesis within the neurovascular unit, might play an important role in the neuro-endocrine-immune (NEI) stress-adaptation system. Recent evidence suggests that VEGF is involved in the pathophysiology of a number of diseases including major depressive disorder (MDD) and is affected by some treatments, including antidepressants. The objective of the study was to investigate the VEGF level variations in MDD patients during antidepressant treatment with duloxetine, a relatively new SNRI.
Cognitive and behavioral manifestations in SARS-CoV-2 infection: not specific or distinctive features?
Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2021

Patients with COVID-19 are increasingly reported to suffer from a wide range of neurological complications, affecting both the central and peripheral nervous system. Among central manifestations, cognitive and behavioral symptoms are to date not exhaustively detailed. Furthermore, it is not clear whether these represent a combination of non-specific complications of a severe systemic disease, not differing from those usually seen in patients suffering from heterogenous pathological conditions affecting the central nervous system, or instead, they are a peculiar expression of COVID-19 neurotropism; in other words, if the infection has a coincidental or causal role in such patients. We examined both hypotheses, reporting opposite points of view, with the aim to stimulate discussion and raise awareness of the topic.
Epilepsy in cerebrovascular diseases: Review of experimental and clinical data with meta-analysis of risk factors.
Epilepsia, 2016

Seizures may occur in close temporal association with a stroke or after a variable interval. Moreover, epilepsy is often encountered in patients with leukoaraiosis. Although early post-stroke seizures have been studied extensively, less attention has been paid to post-stroke epilepsy (PSE) and to epilepsy associated with leukoaraiosis (EAL). The aim of this paper is to review data concerning pathophysiology, prognosis, and treatment of PSE and EAL.
The Interplay of WNT and PPARγ Signaling in Vascular Calcification.
Cells, 2020

Vascular calcification (VC), the ectopic deposition of calcium phosphate crystals in the vessel wall, is one of the primary contributors to cardiovascular death. The pathology of VC is determined by vascular topography, pre-existing diseases, and our genetic heritage. VC evolves from inflammation, mediated by macrophages, and from the osteochondrogenic transition of vascular smooth muscle cells (VSMC) in the atherosclerotic plaque. This pathologic transition partly resembles endochondral ossification, involving the chronologically ordered activation of the β-catenin-independent and -dependent Wingless and Int-1 (WNT) pathways and the termination of peroxisome proliferator-activated receptor γ (PPARγ) signal transduction. Several atherosclerotic plaque studies confirmed the differential activity of PPARγ and the WNT signaling pathways in VC. Notably, the actively regulated β-catenin-dependent and -independent WNT signals increase the osteochondrogenic transformation of VSMC through the up-regulation of the osteochondrogenic transcription factors SRY-box transcription factor 9 (SOX9) and runt-related transcription factor 2 (RUNX2). In addition, we have reported studies showing that WNT signaling pathways may be antagonized by PPARγ activation via the expression of different families of WNT inhibitors and through its direct interaction with β-catenin. In this review, we summarize the existing knowledge on WNT and PPARγ signaling and their interplay during the osteochondrogenic differentiation of VSMC in VC. Finally, we discuss knowledge gaps on this interplay and its possible clinical impact.
Reversal of insular and microstructural nerve abnormalities following effective surgical treatment for trigeminal neuralgia.
Pain, 2015

Classical trigeminal neuralgia (TN) is a severe neuropathic facial pain disorder commonly associated with neurovascular compression at the trigeminal nerve root entry zone (REZ). Neurosurgical interventions can relieve TN pain, but the mechanisms underlying these effects are unknown. We determined whether the abnormalities we previously reported at the REZ of TN patients using diffusion tensor imaging (DTI) and brain gray matter (GM) analyses resolve after effective neurosurgical treatment. Twenty-five patients who underwent either microvascular decompression surgery or Gamma Knife radiosurgery for right-sided TN had magnetic resonance imaging scans before and after treatment and were compared with age-matched controls. Cortical thickness and voxel-based morphometry examined specific brain GM we previously reported as abnormal in TN. White matter metrics of fractional anisotropy (FA), mean, radial, and axial diffusivities (MD, RD, and AD, respectively) were extracted bilaterally from each trigeminal REZ. Before treatment, patients had widespread GM abnormalities including thinner ventral anterior insula (vAI) cortex, and REZ microstructural abnormalities (lower FA, and higher MD, RD, and AD) compared with controls. We considered a 75% reduction in pain as effective treatment. The right vAI was the only GM region that normalized toward the level of healthy controls after effective treatment. At the REZ, effective treatment reversed FA, MD, RD, and AD abnormalities and was correlated with pain relief after treatment. These results demonstrate that treatment can effectively resolve pain by normalizing REZ abnormalities, which may influence vAI abnormalities. Future studies should consider DTI as an adjunct to assess the patient outcome and subtle microstructural changes after treatment.
Olanzapine-induced methylation alters cadherin gene families and associated pathways implicated in psychosis.
BMC neuroscience, 2014

The complex aetiology of most mental disorders involves gene-environment interactions that may operate using epigenetic mechanisms particularly DNA methylation. It may explain many of the features seen in mental disorders including transmission, expression and antipsychotic treatment responses. This report deals with the assessment of DNA methylation in response to an antipsychotic drug (olanzapine) on brain (cerebellum and hippocampus), and liver as a non-neural reference in a rat model. The study focuses on the Cadherin/protocadherins encoded by a multi-gene family that serve as adhesion molecules and are involved in cell-cell communication in the mammalian brain. A number of these molecules have been implicated in the causation of schizophrenia and related disorders.
An inducible Cre mouse for studying roles of the RPE in retinal physiology and disease.
JCI insight, 2021

The retinal pigment epithelium (RPE) provides vital metabolic support for retinal photoreceptor cells and is an important player in numerous retinal diseases. Gene manipulation in mice using the Cre-LoxP system is an invaluable tool for studying the genetic basis of these retinal diseases. However, existing RPE-targeted Cre mouse lines have critical limitations that restrict their reliability for studies of disease pathogenesis and treatment, including mosaic Cre expression, inducer-independent activity, off-target Cre expression, and intrinsic toxicity. Here, we report the generation and characterization of a knockin mouse line in which a P2A-CreERT2 coding sequence is fused with the native RPE-specific 65 kDa protein (Rpe65) gene for cotranslational expression of CreERT2. Cre+/- mice were able to recombine a stringent Cre reporter allele with more than 99% efficiency and absolute RPE specificity upon tamoxifen induction at both postnatal days (PD) 21 and 50. Tamoxifen-independent Cre activity was negligible at PD64. Moreover, tamoxifen-treated Cre+/- mice displayed no signs of structural or functional retinal pathology up to 4 months of age. Despite weak RPE65 expression from the knockin allele, visual cycle function was normal in Cre+/- mice. These data indicate that Rpe65CreERT2 mice are well suited for studies of gene function and pathophysiology in the RPE.
Functional loss of a noncanonical BCOR-PRC1.1 complex accelerates SHH-driven medulloblastoma formation.
Genes & development, 2020

Medulloblastoma is a malignant childhood brain tumor arising from the developing cerebellum. In Sonic Hedgehog (SHH) subgroup medulloblastoma, aberrant activation of SHH signaling causes increased proliferation of granule neuron progenitors (GNPs), and predisposes these cells to tumorigenesis. A second, cooperating genetic hit is often required to push these hyperplastic cells to malignancy and confer mutation-specific characteristics associated with oncogenic signaling. Somatic loss-of-function mutations of the transcriptional corepressor