Visceral fat sympathectomy ameliorates systemic and local stress response related to chronic sleep restriction.

Disturbance of sleep homeostasis encompasses health issues, including metabolic disorders like obesity, diabetes, and augmented stress vulnerability. Sleep and stress interact bidirectionally to influence the central nervous system and metabolism. Murine models demonstrate that decreased sleep time is associated with an increased systemic stress response, characterized by endocrinal imbalance, including the elevated activity of hypothalamic-pituitary-adrenal axis, augmented insulin, and reduced adiponectin, affecting peripheral organs physiology, mainly the white adipose tissue (WAT). Within peripheral organs, a local stress response can also be activated by promoting the formation of corticosterone. This local amplifying glucocorticoid signaling is favored through the activation of the enzyme 11ß-hydroxysteroid dehydrogenase type 1 (11ß-HSD1). In WAT, 11ß-HSD1 activity is upregulated by the sympathetic nervous system, suggesting a link between sleep loss, augmented stress response, and a potential WAT metabolic disturbance. To gain more understanding about this relationship, metabolic and stress responses of WAT-sympathectomized rats were analyzed to identify the contribution of the autonomic nervous system to stress response-related metabolic disorders during chronic sleep restriction. Male Wistar rats under sleep restriction were allowed just 6 h of daily sleep over eight weeks. Results showed that rats under sleep restriction presented higher serum corticosterone, increased adipose tissue 11ß-HSD1 activity, weight loss, decreased visceral fat, augmented adiponectin, lower leptin levels, glucose tolerance impairment, and mildly decreased daily body temperature. In contrast, sympathectomized rats under sleep restriction exhibited decreased stress response (lower serum corticosterone and 11ß-HSD1 activity). In addition, they maintained weight loss, explained by a reduced visceral fat pad, leptin, and adiponectin, improved glucose management, and persisting decline in body temperature. These results suggest autonomic nervous system is partially responsible for the WAT-exacerbated stress response and its metabolic and physiological disturbances.

Feeding during the resting phase causes gastrointestinal tract dysfunction and desynchronization of metabolic and neuronal rhythms in rats.

BACKGROUND: Disrupted circadian rhythms may result from a misalignment between the environmental cycles (due to shift work, sleep restriction, feeding at an unusual time of day) and endogenous rhythms or by physiological aging. Among the numerous adverse effects, disrupted rhythms affect the brain-gut axis, contributing to the pathogenesis of several diseases in the gastrointestinal tract, for example, abdominal pain, constipation, gastric dyspepsia, inflammatory bowel disease, irritable bowel syndrome, and others. METHODS: This study evaluated the rat gastric emptying, gastrointestinal motility, a clock gene, gut hormones, and the neuron activity on the nucleus of tractus solitarius (NTS), area postrema (AP), and the dorsal motor nucleus of the vagus (DMV) in rats with restricted food access to the rest phase for 4 weeks. KEY RESULTS: Our results show that food restricted to the rest light period disturbed the expression pattern of a series of transcripts, including metabolic and circadian regulation. Also, the secretion of gastrointestinal hormones, gastric emptying, intestinal motility, and NTS, AP, and DMV activity were altered. CONCLUSIONS & INFERENCES: These data indicate the importance of the time of the day food is ingested on the regulation of energy balance and the endocrine activity of the stomach and small intestine, emphasizing the importance of food as a powerful circadian synchronizer and an essential factor for the triggering of gastrointestinal diseases and metabolic problems. These findings offer a novel clue regarding the obesity-promoting effect attributed to feeding time and open the possibility of treating this and other intestinal disorders.

Morphological changes and Mitochondrial alterations on Cardiomyocytes exposed to Fluoride.

OBJECTIVE: To evaluate the morphological changes of cardiomyocytes exposed to different sodium fluoride (NaF) concentrations, as well as to evaluate the behavior of the mitochondria. METHODS: Rat H9c2 cardiomyocytes were exposed to NaF at concentrations of 0.5 to 5 mmol/L. The morphology and number of mitochondria in these cells were monitored, and the calcium ion (Ca2+) concentration was determined. RESULTS: Morphological changes were evident in the cells treated with different NaF concentrations, and both the number of mitochondria and the Ca2+ concentration decreased in a dose-dependent manner. CONCLUSION: Sodium fluoride induced morphological damage in cardiomyocytes, decreases the Ca2+ concentration and mitochondrial number.

Leptin and adiponectin regulate the activity of nuclei involved in sleep-wake cycle in male rats.

Epidemiological and experimental evidence recognize a relationship between sleep-wake cycles and adiposity levels, but the mechanisms that link both are not entirely understood. Adipose tissue secretes adiponectin and leptin hormones, mainly involved as indicators of adiposity levels and recently associated to sleep. To understand how two of the main adipose tissue hormones could influence sleep-wake regulation, we evaluated in male rats, the effect of direct administration of adiponectin or leptin in the ventrolateral preoptic nuclei (VLPO), a major area for sleep promotion. The presence of adiponectin (AdipoR1 and AdipoR2) and leptin receptors in VLPO were confirmed by immunohistochemistry. Adiponectin administration increased wakefulness during the rest phase, reduced delta power, and activated wake-promoting neurons, such as the locus coeruleus (LC), tuberomammillary nucleus (TMN) and hypocretin/orexin neurons (OX) within the lateral hypothalamus (LH) and perifornical area (PeF). Conversely, leptin promoted REM and NREM sleep, including increase of delta power during NREM sleep, and induced c-Fos expression in VLPO and melanin concentrating hormone expressing neurons (MCH). In addition, a reduction in wake-promoting neurons activity was found in the TMN, lateral hypothalamus (LH) and perifornical area (PeF), including in the OX neurons. Moreover, leptin administration reduced tyrosine hydroxylase (TH) immunoreactivity in the LC. Our data suggest that adiponectin and leptin act as hormonal mediators between the status of body energy and the regulation of the sleep-wake cycle.

Intervención cognitivo conductual para promover la adhesión al tratamiento médico, recursos psicológicos y calidad de vida en pacientes pediátricos con hemodiálisis en México / Cognitive behavioral intervention to promote adherence to medical treatment, psychological resources, and quality of life in pediatric hemodialysis patients in Mexico

La Enfermedad Renal Crónica [ERC] es un problema de salud pública a nivel mundial. En México, en el año 2018 murieron 13.845 personas por estacausa. El incremento en el riesgo de mortalidad está asociado a la falta de apego al tratamiento. En pacientes pediátricos, una parte importante delmanejo de la enfermedad recae en el cuidador primario. El propósito de la presente investigación fue evaluar la eficacia de una intervención cognitivoconductual para mejorar la adhesión al tratamiento y la calidad de vida, así como promover recursos psicológicos en pacientes pediátricos con ERCen tratamiento de hemodiálisis y al mismo tiempo disminuir la carga en sus cuidadores primarios. El estudio empleó un diseño mixto, longitudinal, queincluyó pre-test, una intervención cognitivo conductual de ocho sesiones en el que se utilizó un manual, una evaluación post-test y un seguimiento a losdos meses. Participaron 5 pacientes pediátricos entre 12 y 17 años de edad y sus cuidadores primarios que asistían a un hospital público de la ciudadde Morelia, Michoacán, en México. Los resultados cuantitativos mostraron una mejora en la adhesión terapéutica, en la calidad de vida global y en losrecursos psicológicos de los pacientes, así como una disminución de la carga en los cuidadores primarios. Los hallazgos cualitativos mostraron que lospacientes lograron entender su padecimiento, expresaron sus emociones respecto a la enfermedad y reconocieron el apoyo de su cuidador primario.Se concluye que el tratamiento cognitivo conductual es una propuesta de intervención eficaz para mejorar las variables de estudio. (AU)

Cognitive behavioral intervention to promote adherence to medical treatment, psychological resources, and quality of life in pediatric hemodialysispatients in Mexico. Chronic Kidney Disease [CKD] is a public health problem worldwide. In Mexico, in 2018 13,845 people died from this cause.The increased risk of mortality is associated with the lack of adherence to treatment. In pediatric patients, an important part of disease managementfall on the primary caregiver. The purpose of the present investigation was to evaluate the efficacy of a cognitive behavioral intervention to improveadherence to treatment and quality of life, as well as to promote psychological resources in pediatric patients with CKD undergoing hemodialysistreatment and at the same time reduce the burden on their primary caregivers. The study used a mixed longitudinal design, with a pretest measurement, an 8-session cognitive-behavioral intervention using a manual, a post-test, and a 2-month follow-up test. Five pediatric patients between 12 and 17 years of age and their primary caregivers who attended a public hospital in the city of Morelia, Michoacán, in Mexico participated. The quantitative results showed an improvement in the therapeutic adherence, in the global quality of life and in the psychological resources of the patients,as well as a decrease in the burden on the primary caregivers. Qualitative findings showed that patients understood their condition, expressed theiremotions about the disease, and recognized the support of their primary caregiver. It is concluded that cognitive behavioral treatment is an effectiveintervention proposal to improve the study variables. (AU)

Temporal dysregulation of hypothalamic integrative and metabolic nuclei in rats fed during the rest phase.

Temporal coordination of organisms according to the daytime allows a better performance of physiological processes. However, modern lifestyle habits, such as food intake during the rest phase, promote internal desynchronization and compromise homeostasis and health. The hypothalamic suprachiasmatic nucleus (SCN) synchronizes body physiology and behavior with the environmental light-dark cycle by transmitting time information to several integrative hypothalamic nuclei, such as the paraventricular nucleus (PVN), dorsomedial hypothalamic nucleus (DMH) and median preoptic area (MnPO). The SCN receives metabolic information mainly via Neuropeptide Y (NPY) inputs from the intergeniculate nucleus of the thalamus (IGL). Nowadays, there is no evidence of the response of the PVN, DMH and MnPO when the animals are subjected to internal desynchronization by restricting food access to the rest phase of the day. To explore this issue, we compared the circadian activity of the SCN, PVN, DMH and MnPO. In addition, we analyzed the daily activity of the satiety centers of the brainstem, the nucleus of the tractus solitarius (NTS) and area postrema (AP), which send metabolic information to the SCN, directly or via the thalamic intergeniculate leaflet (IGL). For that, male Wistar rats were assigned to three meal protocols: fed during the rest phase (Day Fed); fed during the active phase (Night Fed); free access to food (ad libitum). After 21 d, the daily activity patterns of these nuclei were analyzed by c-Fos immunohistochemistry, as well as NPY immunohistochemistry, in the SCN. The results show that eating during the rest period produces a phase advance in the activity of the SCN, changes the daily activity pattern in the MnPO, NTS and AP and flattens the c-Fos rhythm in the PVN and DMH. Altogether, these results validate previous observations of circadian dysregulation that occurs within the central nervous system when meals are consumed during the rest phase, a behavior that is involved in the metabolic alterations described in the literature.

Raman Spectroscopy for Adipose Tissue Assessment in Rat Models of Obesity and Type 1 Diabetes.

Adipose tissue presents structural and functional changes in obesity and type 1 diabetes mellitus (T1DM). In obesity, the size and number of adipocytes and adipokine secretion increases. In T1DM, a loss of adipose tissue suggests changes in the metabolic activity of this tissue. A significant challenge is to find alternative noninvasive methods to evaluate molecular changes in adipose tissue related to obesity and T1DM. Recently, Raman spectroscopy and chemometrics techniques have emerged as a tool for biological tissue analysis. In this work, we propose the use of Raman spectroscopy to characterize spectral differences in adipose tissue from different rat groups (control, obese, and T1DM). The Raman spectra were analyzed using direct band analysis, ratiometric analysis, and chemometric methods (principal component analysis (PCA) and support vector machines (SVMs)). We found that the Raman spectra of obese rats showed significant spectral differences compared to control and diabetic groups related to fatty acids Raman bands. Also, the obese group has a significant decrease in the degree of unsaturation of lipids. The PCA-SVM models showed classification performance ranging from 71.43% to 71.79% accuracy for brown and white adipose tissue samples, respectively. In conclusion, the results demonstrate that Raman spectroscopy can be used as a nondestructive method to assess adipose tissue according to a metabolic condition.

Adherencia al tratamiento en infantes con insuficiencia renal crónica: inclusión del psicólogo al equipo interdisciplinario / Adherence to treatment in children with Chronic Renal Failure: inclusion of the psychologist to the interdisciplinary team

Resumen La enfermedad renal crónica (ERC) constituye una de las principales causas de mortalidad a nivel mundial. Se calcula que en México existen alrededor de 140.000 pacientes con este padecimiento. El presente trabajo tuvo como objetivo comprender los factores que facilitan e inhiben la adherencia al tratamiento de los pacientes pediátricos con ERC, dando énfasis en el abordaje interdisciplinario y en la inclusión del/la psicólogo/a para favorecer la atención integral de los pacientes. Se realizó un estudio descriptivo de tipo cualitativo, por medio de la técnica de entrevista con análisis por categorías. Participaron cuatro profesionales: un médico, una enfermera, una nutrióloga y una psicóloga del Hospital Infantil y de la Clínica de Hemodiálisis Galeno en Morelia, Michoacán, México. Los resultados mostraron la importancia del acompañamiento psicológico al paciente para la aceptación del diagnóstico, el manejo emocional, la adherencia al tratamiento y apoyo social, en especial con su cuidador/a primario. Finalmente, se propone un modelo de atención al paciente con ERC desde un enfoque interdisciplinario.

Abstract Chronic Kidney Disease (CKD) is one of the main causes of mortality worldwide. In Mexico there are around 140,000 patients with this condition. The aim of this research was understand the factors that facilitate and inhibit the adherence to treatment of pediatric patients with CKD, with interdisciplinary approach and the inclusion of the psychologist to promote comprehensive patient care. A descriptive qualitative study was carried out by the interview technique with analysis by categories. Four professionals participated: a doctor, a nurse, a nutritionist and a psychologist of the Children's Hospital and of Galeno Hemodialysis Clinic in Morelia, Michoacán, Mexico. The results showed the importance of psychological support to the patient for the acceptance of the diagnosis, emotional management, adherence to treatment and social support, especially with their primary caregiver. Finally, a model of CKD patient care is proposed from an interdisciplinary approach.

Global goals and suicide prevention in the Circumpolar North.

The purpose of this selective narrative review is to provide an overview of suicide and suicide prevention in the Circumpolar North and the relevance of global strategies and policies to these themes. We conducted a selective review of the English language literature on Arctic Indigenous mental health, suicide, and suicide prevention. We briefly present the social context, epidemiology, and risk and protective factors for suicide in the Arctic, with a focus on Indigenous peoples. We highlight a recent collaborative, intergovernmental response to elevated suicide rates in this region, the Reducing the Incidence of Suicide in Indigenous Groups - Strengths United through Networks Initiative, which used a consensus methodology to identify key outcomes for evaluating suicide prevention interventions in the circumpolar context. In relation to the Sustainable Development Goals, we examine recent policy developments in Indigenous-led suicide prevention and identify opportunities for strengthening policy, community interventions, and research. Globally, suicide prevention is a public health priority, and reducing the number of suicide deaths is a key target for sustainable development. Although overall and country-specific suicide rates have decreased since 1990, there remains wide variation at the regional and local level. This is particularly evident in the Arctic region known as the Circumpolar North, where Indigenous peoples experience marked disparities in suicide risk and suicide deaths compared to non-Indigenous populations. The factors that influence these variations are complex and often rooted in the social and economic consequences of colonization. The integration of science, community-based and Indigenous knowledge, and policies that address upstream risks for suicide will play an important role in suicide prevention alongside the growing number of Indigenous suicide prevention strategies tailored for specific populations.

Nicotine smoking concentrations modulate GABAergic synaptic transmission in murine medial prefrontal cortex by activation of α7* and ß2* nicotinic receptors.

Nicotine is the major addictive component of cigarettes, reaching a brain concentration of ~300 nM during smoking of a single cigarette. The prefrontal cortex (PFC) mechanisms underlying temporary changes of working memory during smoking are incompletely understood. Here, we investigated whether 300 nM nicotine modulates γ-aminobutyric acid (GABA) ergic synaptic transmission from pyramidal neurons of the output layer (V) of the murine medial PFC. We used patch clamp in vitro recording from C57BL/6 mice in the whole-cell configuration to investigate the effect of nicotine on pharmacologically isolated GABAergic postsynaptic currents (IPSCs) in the absence or presence of methyllycaconitine (MLA) or dihydro-ß-erythroidine (DHßE), selective antagonists of α7- and ß2-containing (α7* and ß2*) nicotinic acetylcholine receptors (AChRs), respectively. Our results indicated that nicotine, alone or in the presence of MLA, decreases electrically evoked IPSC (eIPSC) amplitude, whereas in the presence of DHßE, nicotine elicited either an eIPSCs amplitude increase or a decrease. In the presence of DHßE, nicotine increased membrane conductance leaving the paired pulse ratio unchanged in all conditions, suggesting a non-ß2* mediated effect. In the presence of MLA, nicotine decreased the mean spontaneous IPSC (sIPSC) frequency but increased their rise time, suggesting a non-α7* AChR-mediated synaptic modulation. Also, in the presence of DHßE, nicotine decreased both eIPSC rise and decay times. No receptors other than α7* and ß2* appear to be involved in the nicotine effect. Our results indicate that nicotine smoking concentrations modulate GABAergic synaptic currents through mixed pre- and post-synaptic mechanisms by activation of α7* and ß2* AChRs.

Psychometric Properties Of The Highly Sensitive Person Scale In Mexican Population.

Sensory Processing Sensitivity (SPS) is a genetically-determined trait that allows people to notice external and internal subtleties in sensory stimuli easily. This feature provides certain advantages to those who possess it, such as, greater empathy, artistic tastes or skills, also, this people can get greater benefit in circumstances with little exposure to sensory input. However, an unfavorable feature of the trait is an increased vulnerability to development psychopathology. In Mexico there is not an instrument to assess the presence of the SPS, thus, the purpose of this research was to analyze the psychometric properties of the Highly Sensitive Person Scale (HSP Scale) in Mexican population. The results showed that the adaptation of HSP Scale has adequate psychometric properties, so the essential contribution of this study is to provide a reliable and valid instrument that allows to discriminate the presence of the SPS.

Differential Recovery Speed of Activity and Metabolic Rhythms in Rats After an Experimental Protocol of Shift-Work.

The circadian system drives the temporal organization of body physiology in relation to the changing daily environment. Shift-work (SW) disrupts this temporal order and is associated with the loss of homeostasis and metabolic syndrome. In a rodent model of SW based on forced activity in the rest phase for 4 weeks, we describe the occurrence of circadian desynchrony, as well as metabolic and liver dysfunction. To provide better evidence for the impact of altered timing of activity, this study explored how long it takes to recover metabolic rhythms and behavior. Rats were submitted to experimental SW for 4 weeks and then were left to recover for one week. Daily locomotor activity, food intake patterns, serum glucose and triglycerides, and the expression levels of hepatic Pparα, Srebp-1c, Pepck, Bmal1 and Per2 were assessed during the recovery period and were compared with expected data according to a control condition. SW triggered the circadian desynchronization of all of the analyzed parameters. A difference in the time required for realignment was observed among parameters. Locomotor activity achieved the expected phase on day 2, whereas the nocturnal feeding pattern was restored on the sixth recovery day. Daily rhythms of plasma glucose and triglycerides and of Pparα, Pepck and Bmal1 expression in the liver resynchronized on the seventh day, whereas Srebp-1c and Per2 persisted arrhythmic for the entire recovery week. SW does not equally affect behavior and metabolic rhythms, leading to internal desynchrony during the recovery phase.

Arsenic Exposure Contributes to the Bioenergetic Damage in an Alzheimer's Disease Model.

Worldwide, every year there is an increase in the number of people exposed to inorganic arsenic (iAs) via drinking water. Human populations present impaired cognitive function as a result of prenatal and childhood iAs exposure, while studies in animal models demonstrate neurobehavioral deficits accompanied by neurotransmitter, protein, and enzyme alterations. Similar impairments have been observed in close association with Alzheimer's disease (AD). In order to determine whether iAs promotes the pathophysiological progress of AD, we used the 3xTgAD mouse model. Mice were exposed to iAs in drinking water from gestation until 6 months (As-3xTgAD group) and compared with control animals without arsenic (3xTgAD group). We investigated the behavior phenotype on a test battery (circadian rhythm, locomotor behavior, Morris water maze, and contextual fear conditioning). Adenosine triphosphate (ATP), reactive oxygen species, lipid peroxidation, and respiration rates of mitochondria were evaluated, antioxidant components were detected by immunoblots, and immunohistochemical studies were performed to reveal AD markers. As-3xTgAD displayed alterations in their circadian rhythm and exhibited longer freezing time and escape latencies compared to the control group. The bioenergetic profile revealed decreased ATP levels accompanied by the decline of complex I, and an oxidant state in the hippocampus. On the other hand, the cortex showed no changes of oxidant stress and complex I; however, the antioxidant response was increased. Higher immunopositivity to amyloid isoforms and to phosphorylated tau was observed in frontal cortex and hippocampus of exposed animals. In conclusion, mitochondrial dysfunction may be one of the triggering factors through which chronic iAs exposure exacerbates brain AD-like pathology.

RISING SUN: Prioritized Outcomes for Suicide Prevention in the Arctic.

The Arctic Council, a collaborative forum among governments and Arctic communities, has highlighted the problem of suicide and potential solutions. The mental health initiative during the United States chairmanship, Reducing the Incidence of Suicide in Indigenous Groups: Strengths United Through Networks (RISING SUN), used a Delphi methodology complemented by face-to-face stakeholder discussions to identify outcomes to evaluate suicide prevention interventions. RISING SUN underscored that multilevel suicide prevention initiatives require mobilizing resources and enacting policies that promote the capacity for wellness, for example, by reducing adverse childhood experiences, increasing social equity, and mitigating the effects of colonization and poverty.

Global Demand for Natural Resources Eliminated More Than 100,000 Bornean Orangutans.

Unsustainable exploitation of natural resources is increasingly affecting the highly biodiverse tropics [1, 2]. Although rapid developments in remote sensing technology have permitted more precise estimates of land-cover change over large spatial scales [3-5], our knowledge about the effects of these changes on wildlife is much more sparse [6, 7]. Here we use field survey data, predictive density distribution modeling, and remote sensing to investigate the impact of resource use and land-use changes on the density distribution of Bornean orangutans (Pongo pygmaeus). Our models indicate that between 1999 and 2015, half of the orangutan population was affected by logging, deforestation, or industrialized plantations. Although land clearance caused the most dramatic rates of decline, it accounted for only a small proportion of the total loss. A much larger number of orangutans were lost in selectively logged and primary forests, where rates of decline were less precipitous, but where far more orangutans are found. This suggests that further drivers, independent of land-use change, contribute to orangutan loss. This finding is consistent with studies reporting hunting as a major cause in orangutan decline [8-10]. Our predictions of orangutan abundance loss across Borneo suggest that the population decreased by more than 100,000 individuals, corroborating recent estimates of decline [11]. Practical solutions to prevent future orangutan decline can only be realized by addressing its complex causes in a holistic manner across political and societal sectors, such as in land-use planning, resource exploitation, infrastructure development, and education, and by increasing long-term sustainability [12]. VIDEO ABSTRACT.

Evaluación de la imagen corporal en mujeres con cáncer de mama: una revisión sistemática / Body Image of Women with Breast Cancer: A Systematic Review

Resumen La imagen corporal (IC) es la representación subjetiva de la percepción, evaluación, valoración y vivencia del cuerpo que proporciona el sentido de sí mismo como una totalidad. Es afectada cuando existen enfermedades oncológicas que implican cambios corporales. En esta revisión sistemática se identificaron instrumentos susceptibles de usarse en Latinoamérica para evaluar la IC de mujeres con cáncer de mama, analizando 34 artículos publicados en inglés y español del periodo 2004-2014 en bases de libre acceso. Instrumentos originados en Europa y Estados Unidos, tales como la Escala de Imagen Corporal de Hopwood y el módulo QLQ BR 23, desarrollado por la Organización Europea para Investigación y Tratamiento en Cáncer (EORTC), con buenas características psicométricas de validez y confiabilidad, se han utilizado en población latinoamericana. Se valora cómo la IC de mujeres con cáncer de mama afecta su sexualidad, las relaciones de pareja, su autoestima, los estilos de afrontamiento y calidad de vida.

Abstract Body image is the subjective representation of perception, evaluation, assessment and experience of the body that provides the sense of self as a whole. It is affected when passes through diseases, especially when implies physical changes like oncologic diseases.This systematic review identified instruments to assess body image in women with breast cancer, through the analysis of 34 articles published in English and Spanish during the 2004-2014 period in open access repositories. Instruments originated in Europe and the United States, with the psychometric properties of validity and reliability were found.The Body Image Scale of Hopwood and module QLQ BR 23 of the European Organization for Research and Treatment of Cancer were reported in studies in Latin American population. It is valued how the body image of women with breast cancer affects their sexuality, couple relationships, self-steem, coping styles and quality of life affects their sexuality, relationships, self-esteem, coping styles and quality of life.

Food in synchrony with melatonin and corticosterone relieves constant light disturbed metabolism.

Circadian disruption is associated with metabolic disturbances such as hepatic steatosis (HS), obesity and type 2 diabetes. We hypothesized that HS, resulting from constant light (LL) exposure is due to an inconsistency between signals related to food intake and endocrine-driven suprachiasmatic nucleus (SCN) outputs. Indeed, exposing rats to LL induced locomotor, food intake and hormone arrhythmicity together with the development of HS. We investigated whether providing temporal signals such as 12-h food availability or driving a corticosterone plus melatonin rhythm could restore rhythmicity and prevent the metabolic disturbances under LL conditions in male rats. Discrete metabolic improvements under these separate treatments stimulated us to investigate whether the combination of hormone treatment together with mealtime restriction (12-h food during four weeks) could prevent the metabolic alterations. LL exposed arrhythmic rats, received daily administration of corticosterone (2.5 µg/kg) and melatonin (2.5 mg/kg) in synchrony or out of synchrony with their 12-h meal. HS and other metabolic alterations were importantly ameliorated in LL-exposed rats receiving hormonal treatment in synchrony with 12-h restricted mealtime, while treatment out of phase with meal time did not. Interestingly, liver bile acids, a major indication for HS, were only normalized when animals received hormones in synchrony with food indicating that disrupted bile acid metabolism might be an important mechanism for the HS induction under LL conditions. We conclude that food-elicited signals, as well as hormonal signals, are necessary for liver synchronization and that HS arises when there is conflict between food intake and the normal pattern of melatonin and corticosterone.

First integrative trend analysis for a great ape species in Borneo.

For many threatened species the rate and drivers of population decline are difficult to assess accurately: species' surveys are typically restricted to small geographic areas, are conducted over short time periods, and employ a wide range of survey protocols. We addressed methodological challenges for assessing change in the abundance of an endangered species. We applied novel methods for integrating field and interview survey data for the critically endangered Bornean orangutan (Pongo pygmaeus), allowing a deeper understanding of the species' persistence through time. Our analysis revealed that Bornean orangutan populations have declined at a rate of 25% over the last 10 years. Survival rates of the species are lowest in areas with intermediate rainfall, where complex interrelations between soil fertility, agricultural productivity, and human settlement patterns influence persistence. These areas also have highest threats from human-wildlife conflict. Survival rates are further positively associated with forest extent, but are lower in areas where surrounding forest has been recently converted to industrial agriculture. Our study highlights the urgency of determining specific management interventions needed in different locations to counter the trend of decline and its associated drivers.

Cholinergic signaling plasticity maintains viscerosensory responses during Aspiculuris tetraptera infection in mice small intestine.

Intestinal parasites alter gastrointestinal (GI) functions like the cholinergic function. Aspiculuris tetraptera is a pinworm frequently observed in laboratory facilities, which infests the mice cecum and proximal colon. However, little is known about the impact of this infection on the GI sensitivity. Here, we investigated possible changes in spontaneous mesenteric nerve activity and on the mechanosensitivity function of worm-free regions of naturally infected mice with A. tetraptera. Infection increased the basal firing of mesenteric afferent nerves in jejunum. Our findings indicate that nicotinic but not muscarinic receptors, similarly affect spontaneous nerve firing in control and infected animals; these axons are mainly vagal. No difference between groups was observed on spontaneous activity after nicotinic receptor inhibition. However, and contrary to the control group, during infection, the muscarinic signaling was shown to be elevated during mechanosensory experiments. In conclusion, we showed for the first time that alterations induced by infection of the basal afferent activity were independent of the cholinergic function but changes in mechanosensitivity were mediated by muscarinic, but not nicotinic, receptors and specifically by high threshold nerve fibers (activated above 20mmHg), known to play a role in nociception. These plastic changes within the muscarinic signaling would function as a compensatory mechanism to maintain a full mechanosensory response and the excitability of nociceptors during infection. These changes indicate that pinworm colonic infection can target other tissues away from the colon.

Feeding during the rest phase promotes circadian conflict in nuclei that control energy homeostasis and sleep-wake cycle in rats.

Food intake during the rest phase promotes circadian desynchrony, which has been associated with metabolic diseases. However, the link between circadian rhythm and metabolic alterations is not well understood. To investigate this issue, we explored the circadian rhythm of c-Fos immunoreactivity (IR) in rats fed during the day, during the night or with free access to food for 3 weeks. The analysis was focused on the hypothalamic nuclei, which are interconnected and involved in the control of energy homeostasis and/or arousal: lateral hypothalamus (LH), perifornical area, arcuate, ventrolateral pre-optic (VLPO) and tuberomammillary nuclei. The results show that food intake during the rest phase flattened the circadian c-Fos expression in the LH and perifornical area, and induced a phase shift in the VLPO area. In addition, c-Fos expression was analyzed in the orexin and melanin-concentrating hormone (MCH) neurons of the LH, which are involved in the control of food intake and arousal, and in α-melanin-stimulating hormone and neuropeptide Y (NPY) cells in the arcuate nucleus, all of which are involved in feeding-fasting cycles, energy homeostasis and sending projections to the LH. The results indicate that feeding during the rest phase decreased orexin neuron activation in the light in comparison with the other groups. Feeding during this phase also flattened the activity rhythm of MCH and α-melanin-stimulating hormone neurons and increased NPY IR when the light was turned on. This evidence indicates that mealtime differentially affected the hypothalamic nuclei under investigation leading to a circadian conflict that might account for metabolic impairment.