Chronic Deprivation Research Articles

Indominable Color Schemes

This ten-page visual, poetic essay captures my disenfranchisement from my own art and poetry, as well as the continuous instability of my life. I start with parental expectations, symbolized by negative space or violent lines and shapes, pondering the cost of these expectations on the joys and freedom of youth. I move into encounters of transphobic and racist bullying at primary school, a time when it was impossible to bear the terms for such experiences. This is followed by representations of abuse, only retroactively understood throughout the subsequent exploration of it, as well as the chronic deprivation of opportunity that these kinds of injuries cause. The exponential costs, particularly the emotional ones, that incur from the practical losses that come with life are then considered, along with the re-traumatization of simply trying to survive them. Finally, there are discordant uses of space, cluttered and overlayered images and words, alongside isolating negative spaces, to represent the constant feeling of failure, including being broken even during instances of stability or minor success.

Chronic water restriction reduces sensitivity to brain stimulation reward in male and female rats

States of physiological need motivate individuals to seek and consume stimuli that restore homeostatic balance. This goal-directed behavior is driven, in part, by pathways that process reward and are sensitive to changes in physiological state, including the mesolimbic dopamine system. The effects of hunger and its physiological markers have been more widely studied for their role in modulating reward signaling pathways. However, fluid need produces robust goal-directed behavior and has also been shown to affect neural substrates of reward processing. To test how acute and chronic states of thirst might alter reward sensitivity, we used the intracranial self-stimulation (ICSS) rate-frequency paradigm (Carlezon & Chartoff, 2007) with male and female Long Evans rats. We hypothesized that sensitivity to ICSS would increase under an acute need state for water and would decrease under chronic deprivation. We found that acute water deprivation for 22-hours prior to the ICSS session did not alter any parameters of reward sensitivity. To elicit motivated behavior toward water in the absence of physiological need, we chemogenetically activated glutamatergic neurons of the subfornical organ (SFO). Despite eliciting more water consumption than acute deprivation, acute chemogenetic activation of SFO neurons also did not alter reward sensitivity. Finally, subjects underwent a five-day chronic water restriction protocol with daily ICSS sessions to determine the effects of sustained physiological need. Chronic water restriction resulted in reduced sensitivity to ICSS. Together, these results indicate that persistent changes in physiological state alter the responsiveness of reward circuitry that could potentially exacerbate maladaptive reward-seeking behaviors.

Differential Expression of Innate and Adaptive Immune Genes during Acute Physical Exercise in American Quarter Horses.

Overtraining syndrome (OTS) is the reduction in performance due to excess training and lack of proper recovery, which can lead to a chronic deprivation of energy and reduction in the repair of damage that can accumulate over time. Here, the effect of acute, intense physical exercise on the expression of innate and adaptive immune genes in 12 racing-bred American Quarter Horses, after resting for 3 days and immediately after intense exercise for 1.8 miles were compared. The expression of 84 genes related to innate and adaptive immune responses was analyzed. Significant variation among individuals and between sexes was observed. The analysis showed that five genes were differentially expressed in both females and males, three only in females, and two in males. The upregulated genes were IL13 (male only), CCR4 (female only), TLR6, TLR9 (female only), NFKBIA, CXCR3, and TLR4, while the downregulated genes were IL6 (female only), CD4 (male only), and MYD88. The three main pathways containing genes that were affected by acute, intense physical exercise were Th1 and Th2 cell differentiation, and the NF-kappa B and chemokine signaling pathways, suggesting the activation of the proinflammatory responses as a result of the stress from the acute exercise. Gene expression could be used to assess indications of OTS.

0009 Interindividual variation and extended wakefulness in sleepiness after acute and chronic sleep deprivation

Abstract Introduction Sleepiness is a behavioural consequence of sleep pressure and is associated with negative outcomes with interindividual variation, possibly related to central sleep mechanisms. However, there is a lack of evidence linking progressive sleep need and sleepiness with factors of individual variability, which could be tested by total acute and chronic sleep deprivation. Thus, the objective of the study was to investigate the development of sleepiness in sleep deprived mice. Methods Male C57BL/6J mice were distributed in sleep deprivation, sleep rebound and control groups. Animals underwent acute sleep deprivation for 3, 6, 9 or 12 hours or chronic sleep deprivation for 6 hours for 5 consecutive days. Sleep rebound groups had a sleep opportunity for 1, 2, 3, or 4 hours after acute sleep deprivation or 24 hours after chronic sleep deprivation. During the protocols, sleep attempts were counted to calculate a sleepiness index. After euthanasia, blood was collected for corticosterone assessment. Results Using the average of group sleep attempts, it was possible to differentiate between sleepy (mean>group average) and resistant animals (mean<group average). Resistant mice were more frequent in all settings. Individual variation accounted for 52% of sleepiness variance during chronic sleep deprivation and extended wakefulness explained 68% of sleepiness variance during acute sleep deprivation. A normal corticosterone peak was observed at the start of the dark phase, independent of sleep deprivation. Conclusion Different profiles of sleepiness emerged in sleep deprived mice. Sleep deprivation was the main factor for sleepiness during acute sleep deprivation whereas in chronic deprivation individual variation was more relevant. Support (If Any) Our studies are supported by the following funding agencies: AFIP (Associação Fundo de Incentivo à Pesquisa), São Paulo Research Foundation (FAPESP #2017/18455-5 to GLF), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - Brasil (CAPES - Finance Code 001 to GLF), and CNPq (fellowships to MLA and ST; #169040/2017-8, and #141445/2021-1 to GLF). This study received indirect funding from AFIP and CNPq, which support the department in which the project was conducted.

Sleepiness profiles in mice submitted to acute and chronic sleep deprivation

SummarySleepiness is a behavioural consequence of sleep pressure, which shows interindividual variation, a characteristic possibly related to central sleep mechanisms. However, there is a lack of evidence linking progressive sleep need and sleepiness with factors of individual variability, which could be tested by total acute and chronic sleep deprivation. Thus, the objective of the study was to investigate the development of sleepiness in sleep deprived mice. Male C57BL/6J mice were distributed in sleep deprivation, sleep rebound and control groups. Animals underwent acute sleep deprivation for 3, 6, 9 or 12 h or chronic sleep deprivation for 6 h for 5 consecutive days. Sleep rebound groups had a sleep opportunity for 1, 2, 3, or 4 h after acute sleep deprivation or 24 h after chronic sleep deprivation. During the protocols, sleep attempts were counted to calculate a sleepiness index. After euthanasia, blood was collected for corticosterone assessment. Using the average of group sleep attempts, it was possible to differentiate between sleepy (mean>group average) and resistant animals (mean<group average). Resistant mice were more frequent in all protocols. Individual variation accounted for 52% of sleepiness variance during chronic sleep deprivation and extended wakefulness explained 68% of sleepiness variance during acute sleep deprivation. A normal corticosterone peak was observed at the start of the dark phase, independent of sleep deprivation. Different profiles of sleepiness emerged in sleep deprived mice. Sleep deprivation was the main factor for sleepiness during acute sleep deprivation whereas in chronic deprivation individual variation was more relevant.

Is mother's financial autonomy associated with stunting among children aged 7-35 months: An empirical study from India.

Stunting depicts chronic deprivation and is a huge public health problem in several developing countries. Considering the sociocultural and sociodemographic factors of India, we aimed to examine the relationship between maternal autonomy and stunting among children <35 months. We have used the data from the latest round of National Family health survey conducted in 2015-16. The main exposure variable was women's autonomy which are represented in our study by the four dimensions- decision-making, physical mobility, financial autonomy, attitudes towards domestic violence, the main predictor variable was stunting among children. Chi-square analysis, univariate and multivariable binary logistic regression analysis were performed to find the association of childhood stunting and women's autonomy. The results were reported at 5% level of significance. All the autonomy variables have shown a significant association with child stunting at 5% level of significance. The unadjusted odds of stunting were found to be significant with respect to all the four dimensions of autonomy variables except physical autonomy. However, after adjusting for other explanatory factors attenuated these relationships and made them statistically insignificant except for women's economic autonomy (AOR = 0.91; 95% C.I.-(0.85, 0.98)) which was found to be significantly affecting the child's status of stunting. Our study reinforces that maternal autonomy is a significant predictor of childhood stunting. Hence, we recommend that policy makers, while designing interventions and policies, must address the socioeconomic inequalities at the community level while devising ways to improve women's empowerment. As it has far-reaching consequences on the nutrition status of the upcoming generations.

Effect of androgen deprivation therapy on bone mineral density in patients with prostate cancer.

Objectives:To access the effects of acute and chronic Androgen Deprivation Therapy on Bone Marrow Density and related bone markers; to compare the bone loss among the patients who terminated GnRH use and control group (not given ADP therapy at all) with the ones with acute or chronic Androgen Deprivation Therapy.Methods:A cross-sectional study was conducted in the Oncology Department of Nishtar Medical University & Hospital Multan for one year. Bone mineral density of the entire body, 1/3rd distal radius, ultra-distal forearm, femoral neck, and lumbar spine, was measured in 40 patients diagnosed with non-metastatic prostate cancer at baseline for the duration of six months. They were categorized into four groups: (i) acute ADT (less than six months of treatment; (ii) chronic ADT (greater than six months of treatment; (iii) former ADT; and (iv) no ADT (placebo groups). Quantitative measures of bone metabolism marker, including C-terminal cross-linking telopeptide of type I collagen (CTX) and procollagen type I N-terminal propeptide (PINP) was done.Results:The cross-sectional analysis showed that BMD dropped significantly in more in patients with former ADT or control groups as compared to chronic ADT. At the 6th month assessment, a significant decline in ultra-distal forearm BMD was demonstrated in patients from both acute and chronic ADT groups (4.05% and 2.54%, P = .001 and .016, respectively). Total body BMD was significantly reduced among those on acute treatment (2.91%, p=0.022). In the former ADT group, a significant increase of BMD was observed in the femoral neck and lumbar spine bones (1.60 % and 2.85%, P = .001 and .0064, respectively). The difference of changes in BMD of the acute and chronic groups was not significant. The levels of PINP and CTX levels were significantly increased in an chronic and acute group than in placebo or former ADT groups.Conclusion:Chronic and acute ADT users experience similar changes in BMD levels but reversibility of BMD can be achieved on withdrawal of treatment. Similarly disturbed bone metabolism markers come back in range on withdrawal of treatment.

Factors Associated With Chronic Lack of Energy In Pregnant Women

According to who (world health organization) the incidence of malnutrition in pregnant women ranges from 20-48% maternal mortality (AKI) in central Java during 2012 reached 678 (5.6%) cases, tending to increase compared to the previous year. In 2011 the number of AKI was recorded at 668 (5.5%) cases from 592,000 pregnant women, while in 2012 the number of AKI increased to 678 (5.6%) cases from 604,000 pregnant women. The purpose of this study was to find out the factors associated with the incidence of chronic energy deprivation (KEK) in pregnant women in the working area of Ponre Health Center of Bulukumba Regency in 2020. The research method used is quantitative research where this research uses research design with cross design sectional study. The results showed that there was a relationship between knowledge levels and income levels with the incidence of chronic energy deprivation (KEK) in pregnant women in Ponre Health Center of Bulukumba Regency, but there was no relationship between paritas or the number of pregnancies and the incidence of chronic less energy (KEK). Based on the results of research that has been done, taking into account the limitations that exist is expected for future research to improve these things and expand the sample of research not only focusing on pregnant women researchers can also examine adolescents and also partus mothers who experience chronic lack of energy (KEK).

Wellbeing of Russian Professionals: Dynamics and Specificity

The paper is devoted to the issue of Russian professionals' life changes in the 2010s and the role of human capital in these processes. Life changes are analyzed by identifying mobility cases within three social stratifications by income, presence of signs of privilege or deprivation, and subjectively perceived position in society. For these purposes, we use panel data of RLMS HSE research for 2014-2018 yy. Trajectories of mobility are revealed by using of «Group based trajectory modeling» method. The results show that life stability dominates over mobility. Professionals still have risks of chronic poverty and chronic deprivation, although these risks are rare for them. They also have chances of objectively measuring sustainable well-being by income and privilege criteria. However, even those who have stayed rich and privileged over the years do not feel that they occupy the highest positions in social structure. It is shown that human capital plays a high role in life chances on sustainable privilege and a high-income level. An obstacle on the path to wealth is the dependency burden. The highest risks of poverty characterize young and middle-aged professionals, while professionals who reach retirement age have the highest chances to be rich. Thus, it is a good strategy to continue labor activity in retirement age. It was revealed that parental education significantly increases chances to achieve privilege position in Russian society. These odds are heavily influenced by composite rents. It is also shown that one of the major factors that create unequal chances of gaining high position in society (both in terms of income and privilege) is settlement inequalities. Despite a quite prosperous life dynamics measured by objective indicators, every third professional feels chronically poor or felt a sharp impoverishment during these years. These subjective assessments are weakly correlated with the quality of human capital and observed in all age categories. We associate this phenomenon with two factors: 1) "negative stabilization" in the 2010s and 2) with the fact that chances for objective well-being are confined mainly to the structural factor of settlement inequality. The position of professionals is often contradictory. The groups of privileged and wealthy professionals have little overlap in composition. In modern Russia, wealth does not imply a privileged position in society and vice versa. The same is true for poverty and deprivation. Absolute well-being, i.e., stable occupation of the highest positions in all three structural positions, is practically unavailable to Russian professionals.

The effect of deprivation on depression across different age groups in Korea

AbstractThis study aimed to verify whether deprivation is experienced differently across different age groups and whether these differences change the effect of deprivation on depression. In this study, the CES‐D 11 scale was used to measure depression. Additionally, to verify the relationship between deprivation and depression by age group, logistics analysis was conducted. This study analyzed the survey data of 4,000 individuals from Korea; respondents were classified into four age groups: ≤34, 35–49, 50–64, and ≥65 years old. The results showed that there was a significant relationship between deprivation and depression and that specific areas of deprivation affected depression differently for each age group. The deprivation ratios of older individuals were higher in all areas. Further, the deprivation ratio of the ≤34 group in housing and living conditions was higher than that of the other groups. Additionally, respondents in the 50–64 and the ≥65 groups were alienated from the social security network, which poses an increased risk for chronic deprivation or poverty. The results of this study suggest that policies and practical interventions are needed, taking into account that the effects of absolute and relative deprivation on depression vary by age group.

Mechanisms of vitamin A metabolism and deficiency in the mammalian and fly visual system

Vitamin A deficiency can cause human pathologies that range from blindness to embryonic malformations. This diversity is due to the lack of two major vitamin A metabolites with very different functions: the chromophore 11-cis-retinal (vitamin A aldehyde) is a critical component of the visual pigment that mediates phototransduction, while the signaling molecule all-trans-retinoic acid regulates the development of various tissues and is required for the function of the immune system.Since animals cannot synthesize vitamin A de novo, they must obtain it either as preformed vitamin A from animal products or as carotenoid precursors from plant sources. Due to its essential role in the visual system, acute vitamin A deprivation impairs photoreceptor function and causes night blindness (poor vision under dim light conditions), while chronic deprivation results in retinal dystrophies and photoreceptor cell death. Chronic vitamin A deficiency is the leading cause of preventable childhood blindness according to the World Health Organization. Due to the requirement of vitamin A for retinoic acid signaling in development and in the immune system, vitamin A deficiency also causes increased mortality in children and pregnant women in developing countries.Drosophila melanogaster is an excellent model to study the effects of vitamin A deprivation on the eye because vitamin A is not essential for Drosophila development and chronic deficiency does not cause lethality. Moreover, genetic screens in Drosophila have identified evolutionarily conserved factors that mediate the production of vitamin A and its cellular uptake. Here, we review our current knowledge about the role of vitamin A in the visual system of mammals and Drosophila melanogaster. We compare the molecular mechanisms that mediate the uptake of dietary vitamin A precursors and the metabolism of vitamin A, as well as the consequences of vitamin A deficiency for the structure and function of the eye.

PERFORMANCE OF THE STORY OF RUTH TO PROMOTE HEALING FROM “TOWNSHIP TRAUMA”

Many children in South Africa grow up in townships, where they are exposed to violence, drugs, gangs, and poverty. Difficulties in their home situations result in many of them lacking soft skills that enable a person to thrive (such as self-esteem, self-confidence, and the ability to communicate well). This chronic deprivation is an ongoing trauma which requires intervention to promote healing. Using the arts and sport to provide such intervention has been found to be successful, but theorists posit that drama could have value for social and emotional learning. This study tests that hypothesis: two groups (a group of grade 7 learners and a group of adults from a Bible-study fellowship) participate in a dramatic presentation of the biblical story of Ruth. Over a period of six months, the participants meet weekly (in their respective groups) for an hour to learn the story and find their way of expressing it. Three performances before various audiences are presented. To highlight emotional issues in the story, a jester is included in the cast, with the role of interrupting the story at appropriate places and asking the audience questions as to the motivations and moods of the characters. This prompts the audience to reflect on their own emotional responses to various difficult situations with which they readily identify. By considering their own viewpoints, and those of others, audience members are stretched in their social and emotional learning. Moreover, it is apparent that, through the drama experience, the actors gain significantly in self-esteem, self-confidence, and their ability to speak in public before an audience (even adult strangers). This article provides a stimulus for using performance of a biblical text to explore options for dealing with traumatic situations.

Long-Term Shaping of Corticostriatal Synaptic Activity by Acute Fasting.

Food restriction is a robust nongenic, nonsurgical and nonpharmacologic intervention known to improve health and extend lifespan in various species. Food is considered the most essential and frequently consumed natural reward, and current observations have demonstrated homeostatic responses and neuroadaptations to sustained intermittent or chronic deprivation. Results obtained to date indicate that food deprivation affects glutamatergic synapses, favoring the insertion of GluA2-lacking α-Ammino-3-idrossi-5-Metil-4-idrossazol-Propionic Acid receptors (AMPARs) in postsynaptic membranes. Despite an increasing number of studies pointing towards specific changes in response to dietary restrictions in brain regions, such as the nucleus accumbens and hippocampus, none have investigated the long-term effects of such practice in the dorsal striatum. This basal ganglia nucleus is involved in habit formation and in eating behavior, especially that based on dopaminergic control of motivation for food in both humans and animals. Here, we explored whether we could retrieve long-term signs of changes in AMPARs subunit composition in dorsal striatal neurons of mice acutely deprived for 12 hours/day for two consecutive days by analyzing glutamatergic neurotransmission and the principal forms of dopamine and glutamate-dependent synaptic plasticity. Overall, our data show that a moderate food deprivation in experimental animals is a salient event mirrored by a series of neuroadaptations and suggest that dietary restriction may be determinant in shaping striatal synaptic plasticity in the physiological state.

Addressing the tissue of chronic deprivation of a cardiac ventricle

Heart failure is also termed as congestive heart failure (CHF), the congestive cardiac failure (CCF) degenerates cordis is when the heart is unable to pump enough to maintain the same blood flow to connects the body tissues' needs for metabolism. Signs and symptoms of the heart failure is generally including shortness of breath, excessive tiredness, leg swelling etc. The shortness of the breath is usually worse with exercise or while lying down and may wake the person at night. A limited ability to exercise is also a common characteristic feature of cardiac system. The chest pain including an angina, does it not typically occur due to heart failure.

Activity-Dependent Mitochondrial Plasticity and Mitoproteome are Dysregulated in Fragile X Syndrome

Homeostatic plasticity is necessary for the construction and maintenance of functional neuronal networks and becomes disrupted in certain neurodevelopmental disorders. Principal molecular mechanisms required for or modified by homeostatic plasticity are not well understood. We recently reported that homeostatic plasticity induced by activity deprivation is dysregulated in cortical neurons from Fragile X Mental Retardation protein (FMRP) knockout mice (Bulow et al. 2019). These findings suggested to us that proteins responsive to both activity deprivation and modulated by FMRP expression would be robust putative pathways necessary for or modified by homeostatic plasticity. Here, we used unbiased quantitative mass spectrometry to quantify steady-state proteome changes following chronic activity deprivation in wild type and Fmr1-/y cortical neurons. We found that most proteome hits responsive to both activity deprivation and the Fmr1-/y genotype were annotated to mitochondria. Surprisingly, we observed that Fmr1-/y neurons showed exaggerated changes in the expression of mitochondrial proteins following activity deprivation. We identified significant, but compartment specific, changes in the mitochondrial morphology and membrane polarization in dendrites and axons of wild type neurons following activity deprivation. However, these compartmentalized changes were already present in Fmr1-/y neurons at baseline and remained insensitive to activity deprivation. Our findings suggest that mitochondria are required and modified during the induction, establishment or maintenance of homeostatic plasticity. Loss of FMRP exaggerates changes in the mitoproteome during activity deprivation, but Fmr1-/y neurons fail to appropriately regulate mitochondrial morphology and function in an activity dependent and compartmentalized manner. We propose that abnormal compartmentalized mitochondrial plasticity contributes to neurodevelopmental disorders.

Abstract 248: Targeting compensatory metabolic pathways: Novel approaches to overcome resistance to glutaminase inhibition in NF1 driven malignant peripheral nerve sheath tumors

Abstract Acquired therapeutic resistance to targeted therapies has garnered a lot of attention owing to its clinical relevance in cancer research. In addition to acquired mutations as part of the resistant mechanism, key metabolic pathways are often dysregulated in resistant cells. One such important metabolic pathway mediated by glutamine, is critical for the survival and proliferation of many cancer cells. In this study, we studied the mechanism of development of acquired resistance to glutaminase (GLS1) inhibitor, CB-839, in NF1 driven MPNST cell lines. While NF1-null cell lines ST8814 and S462 were sensitive to CB-839, wild-type NF1 bearing cell line, STS26T did not show inhibition of proliferation by CB-839. To develop therapeutic resistance, we treated NF1-null S462 cell line by chronic exposure to CB-839 in a dose escalating manner. Cell viability assay and western blot analysis confirmed abrogation of CB-839 mediated inhibition of proliferation and induction of apoptosis in resistant cell lines. Arginosuccinate synthetase (ASS1), a key metabolic enzyme, has previously been shown to be upregulated in response to chronic pharmacologic arginine deprivation. Western blot analysis in CB-839 sensitive versus resistant S462 cell lines showed upregulation of ASS1 expression. Wild type NF1 carrying cell line STS26T also showed high levels of ASS1 expression. To test whether upregulated ASS1 levels contribute to the development of resistance, we carried out siRNA mediated knockdown of ASS1 in both CB-839 resistant S462 cell line and STS26T cell line. Knockdown of ASS1 resulted in inhibition of proliferation in STS26T cell line as well as restoring sensitivity of resistant S462 cell line to CB-839. Furthermore, overexpression of ASS1 in parental CB-839 sensitive S462 cell line resulted in diminished response to CB-839 mediated inhibition of proliferation. Metabolic profiling of parental versus resistant S462 cell lines showed drastically reduced levels of succinate, a key metabolic intermediate in the TCA cycle, suggesting that upregulation of ASS1 in the resistant cell line results in a cross talk between glutamine and arginine pathways thereby feeding the glutamine into urea cycle rather than TCA cycle. Global histone profiling in CB-839 resistant S462 cell line showed a marked decrease in the repressive methylation marks H3K9me3 as well as H3K27me3. Rescue experiment using exogenous succinate indeed resulted in restoring suppressed H3K9me3 signal in the CB-839 resistant cell line. Taken together, our data strongly suggests that compensatory metabolic pathways such as ASS1 can be used as a means of developing therapeutic resistance to glutaminase inhibition. Targeting of such compensatory pathways is a novel potential approach that needs to be evaluated further in the treatment of drug resistant NF1 driven MPNST tumors. Citation Format: Tahir N. Sheikh, Chao Lu, Gary K. Schwartz. Targeting compensatory metabolic pathways: Novel approaches to overcome resistance to glutaminase inhibition in NF1 driven malignant peripheral nerve sheath tumors [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 248.

Improvement in cardiac function of ovariectomized rats by antioxidant tempol

A rise in heart disease incidence in women after menopause has led to investigations into the role of female sex hormones on cardiac function. Although various adverse changes in cardiac contractile function following loss of female sex hormones have been reported, a clear mechanism of action has never been characterized. In order to examine whether an elevation in oxidative stress is a major cause of cardiac contractile dysfunction after female sex hormone deprivation, cardiac functions of ovariectomized rats with and without supplementation of superoxide scavenger tempol were compared to those of sham-operated controls. Chronic deprivation of female sex hormones reduced total oxidative capacity and increased plasma carbonyl protein content. Tempol supplementation of ovariectomized rats significantly ameliorated plasma oxidative stress status. Echocardiography demonstrated a significant decrease in left ventricular ejection fraction in ovariectomized rats, which was completely prevented by tempol supplementation. Decreased myocardial contractility occurs with reduced maximum myofilament force of contraction and amplitude of transient intracellular Ca2+ concentration, both phenomena completely attenuated by tempol supplementation. However, tempol only partially prevented shift of heart myosin heavy chain from dominant α-to β-isoform of ovariectomized rats. Immunoblot analysis of protein carbonylation indicated that tempol supplementation significantly reduced the level of cardiac myofibrillar proteins oxidation increased in ovariectomized rat heart. Taken together, the results indicate changes of cardiac contractile machinery following loss of female sex hormones were, in part, due to an increase in oxidative stress, and antioxidant supplementation could be considered another potential prevention measure in postmenopausal women.

P164 Association between chronic microbial infection and deprivation in a north-west cystic fibrosis centre

P164 Association between chronic microbial infection and deprivation in a north-west cystic fibrosis centre

0270 Somnolence Profiles in Mice Submitted to Acute and Chronic Sleep Deprivation

Abstract Introduction Sleepiness is a behavioral marker of homeostatic sleep regulation and is related to several negative outcomes with interindividual variation, which may amount to central sleep mechanisms. However, there is a lack of evidence linking progressive sleep need and sleepiness with factors of individual variability, which could be tested by acute and chronic sleep deprivation. Thus, the study objective was to investigate the development of sleepiness in sleep deprived mice. Methods C57BL/6J male mice (n=340) were distributed in 5 sleep deprivation groups, 5 sleep rebound groups and 10 control groups. Animals underwent acute total sleep deprivation for 3, 6, 9 or 12 hours or chronic sleep deprivation for 6 hours for 5 consecutive days. Sleep rebound groups had the opportunity to sleep for 1, 2, 3, 4 hours after acute sleep deprivation or 24 hours after chronic sleep deprivation. During the protocol, sleep attempts were counted as a sleepiness index. After euthanasia, blood was collected for corticosterone assessment. Results Using the average group sleep attempts, it was possible to differentiate between sleepy (mean&amp;gt;group average) and resistant to sleepiness animals (mean&amp;lt;group average). Frequency of resistant mice was 65%, 56%, 56% and 53% for 3, 6, 9 and 12 hours of acute sleep deprivation, respectively, and 74% in chronic sleep deprivation. 52% of the sleepiness variance might be explained by individual variation during chronic sleep deprivation and 68% of sleepiness variance during acute sleep deprivation was attributed to extended wakefulness. A normal corticosterone zenith was observed at the start of the dark phase, independent of sleep deprivation. Conclusion Different degrees of sleepiness in sleep deprived mice were verified. Sleep deprivation per se was the main factor explaining sleepiness during acute sleep deprivation whereas in chronic deprivation individual variation was more relevant. Support This work was financially supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) (#2017/18455-5), Coordenação de Aperfeiçoamento de Pessoal Nível Superior (CAPES) - grant code 001, ConselhoNacional de Desenvolvimento Científico e Tecnológico (CNPq) (#169040/2017–8)and Associação Fundo de Incentivo à Pesquisa (AFIP).

17\u03b1 Estradiol promotes plasticity of spared inputs in the adult amblyopic visual cortex

The promotion of structural and functional plasticity by estrogens is a promising approach to enhance central nervous system function in the aged. However, how the sensitivity to estrogens is regulated across brain regions, age and experience is poorly understood. To ask if estradiol treatment impacts structural and functional plasticity in sensory cortices, we examined the acute effect of 17α-Estradiol in adult Long Evans rats following chronic monocular deprivation, a manipulation that reduces the strength and selectivity of deprived eye vision. Chronic monocular deprivation decreased thalamic input from the deprived eye to the binocular visual cortex and accelerated short-term depression of the deprived eye pathway, but did not change the density of excitatory synapses in primary visual cortex. Importantly, we found that the classical estrogen receptors ERα and ERβ were robustly expressed in the adult visual cortex, and that a single dose of 17α-Estradiol reduced the expression of the calcium-binding protein parvalbumin, decreased the integrity of the extracellular matrix and increased the size of excitatory postsynaptic densities. Furthermore, 17α-Estradiol enhanced experience-dependent plasticity in the amblyopic visual cortex, by promoting response potentiation of the pathway served by the non-deprived eye. The promotion of plasticity at synapses serving the non-deprived eye may reflect selectivity for synapses with an initially low probability of neurotransmitter release, and may inform strategies to remap spared inputs around a scotoma or a cortical infarct.