Stress-activated brain-gut circuits disrupt intestinal barrier integrity and social behaviour.

Chronic stress underlies the etiology of both major depressive disorder (MDD) and irritable bowel syndrome (IBS), two highly prevalent and debilitating conditions with high rates of co-morbidity. However, it is not fully understood how the brain and gut bi-directionally communicate during stress to impact intestinal homeostasis and stress-relevant behaviours. Using the chronic social defeat stress (CSDS) model, we find that stressed mice display greater intestinal permeability and circulating levels of the endotoxin lipopolysaccharide (LPS) compared to unstressed control (CON) mice. Interestingly, the microbiota in the colon also exhibit elevated LPS biosynthesis gene expression following CSDS. Additionally, CSDS triggers an increase in pro-inflammatory colonic IFNγ+ Th1 cells and a decrease in IL4+ Th2 cells compared to CON mice, and this gut inflammation contributes to stress-induced intestinal barrier permeability and social avoidance behaviour. We next investigated the role of enteric neurons and identified that noradrenergic dopamine beta-hydroxylase (DBH)+ neurons in the colon are activated by CSDS, and that their ablation protects against gut pathophysiology and disturbances in social behaviour. Retrograde tracing from the colon identified a population of corticotropin-releasing hormone-expressing (CRH+) neurons in the paraventricular nucleus of the hypothalamus (PVH) that innervate the colon and are activated by stress. Chemogenetically activating these PVH CRH+ neurons is sufficient to induce gut inflammation, barrier permeability, and social avoidance behaviour, while inhibiting these cells prevents these effects following exposure to CSDS. Thus, we define a stress-activated brain-to-gut circuit that confers colonic inflammation, leading to impaired intestinal barrier function, and consequent behavioural deficits.

The Neurobiology of Eating Behavior in Obesity: Mechanisms and Therapeutic Targets: A Report from the 23rd Annual Harvard Nutrition Obesity Symposium.

Obesity is increasing at an alarming rate. The effectiveness of currently available strategies for the treatment of obesity (including pharmacologic, surgical, and behavioral interventions) is limited. Understanding the neurobiology of appetite and the important drivers of energy intake (EI) can lead to the development of more effective strategies for the prevention and treatment of obesity. Appetite regulation is complex and is influenced by genetic, social, and environmental factors. It is intricately regulated by a complex interplay of endocrine, gastrointestinal, and neural systems. Hormonal and neural signals generated in response to the energy state of the organism and the quality of food eaten are communicated by paracrine, endocrine, and gastrointestinal signals to the nervous system. The central nervous system integrates homeostatic and hedonic signals to regulate appetite. Although there has been an enormous amount of research over many decades regarding the regulation of EI and body weight, research is only now yielding potentially effective treatment strategies for obesity. The purpose of this article is to summarize the key findings presented in June 2022 at the 23rd annual Harvard Nutrition Obesity Symposium entitled "The Neurobiology of Eating Behavior in Obesity: Mechanisms and Therapeutic Targets." Findings presented at the symposium, sponsored by NIH P30 Nutrition Obesity Research Center at Harvard, enhance our current understanding of appetite biology, including innovative techniques used to assess and systematically manipulate critical hedonic processes, which will shape future research and the development of therapeutics for obesity prevention and treatment.

D1 and D2 neurons in the nucleus accumbens enable positive and negative control over sugar intake in mice.

Although the consumption of carbohydrates is needed for survival, their potent reinforcing properties drive obesity worldwide. In turn, sugar overconsumption reveals a major role for brain reward systems in regulating sugar intake. However, it remains elusive how different cell types within the reward circuitries control the initiation and termination of sugary meals. Here, we identified the distinct nucleus accumbens cell types that mediate the chemosensory versus postprandial properties of sweet sugars. Specifically, D1 neurons enhance sugar intake via specialized connections to taste ganglia, whereas D2 neurons mediate the termination of sugary meals via anatomical connections to circuits involved in appetite suppression. Consistently, D2, but not D1, neurons partially mediate the satiating effects of glucagon-like peptide 1 (GLP-1) agonists. Thus, these nucleus accumbens cell types function as a behavioral switch, enabling positive versus negative control over sugar intake. Our study contributes to unveiling the cellular and circuit substrates of sugar overconsumption.

Identification of central amygdala and trigeminal motor nucleus connectivity in humans: An ultra-high field diffusion MRI study.

The neuroanatomical circuitry of jaw muscles has been mostly explored in non-human animals. A recent rodent study revealed a novel circuit from the central amygdala (CeA) to the trigeminal motor nucleus (5M), which controls biting attacks. This circuit has yet to be delineated in humans. Ultra-high diffusion-weighted imaging data from the Human Connectome Project (HCP) allow in vivo delineation of circuits identified in other species-for example, the CeA-5M pathway-in humans. We hypothesized that the CeA-5M circuit could be resolved in humans at both 7 and 3 T. We performed probabilistic tractography between the CeA and 5M in 30 healthy young adults from the HCP database. As a negative control, we performed tractography between the basolateral amygdala (BLAT) and 5M, as CeA is the only amygdalar nucleus with extensive projections to the brainstem. Connectivity strength was operationalized as the number of streamlines between each region of interest. Connectivity strength between CeA-5M and BLAT-5M within each hemisphere was compared, and CeA-5M circuit had significantly stronger connectivity than the BLAT-5M circuit, bilaterally at both 7 T (all p < .001) and 3 T (all p < .001). This study is the first to delineate the CeA-5M circuit in humans.

Recurrent American visceral leishmaniasis in a kidney transplant recipient: A case report / Leishmaniasis visceral americana recidivante en un trasplantado renal: reporte de caso

Introduction: American visceral leishmaniasis (AVL) is a neglected tropical disease that causes severe conditions in immunosuppressed patients such as kidney transplant recipients. In these individuals, the infection can be associated with renal graft dysfunction and loss. Objective: To describe the case of a female kidney transplant recipient assisted at the Hospital das Clínicas of Marília Medical School, who died probably as a result of hemodialysis-related complications after graft loss due to treatment toxicity of her underlying disease. Clinical case: A 22-year-old patient, resident in an endemic region of AVL, immunosuppressed due to renal transplantation, who evolved to graft loss after successive relapses, treatment and drug prophylaxis for AVL. With the interruption of immunosuppressive therapy and return to dialysis, amastigote forms were not observed in a bone marrow aspirate smears. However, after one year, she progressed to death due to a cerebrovascular accident resulting from comorbidities. Conclusions: It is described a rare case of successive relapses of AVL and difficult medical decision due to the therapeutic impasse between the use of immunosuppressive drugs for renal graft maintenance and treatment for the parasitic disease. The parasitological control was observed with the immunosuppression suspension, demonstrating the importance of a competent immune system and the adjuvant of specific drugs for the disease control(AU)

Introducción: La leishmaniasis visceral americana (LVA) es una enfermedad tropical desatendida causante de cuadros graves en pacientes inmunodeprimidos, tales como los trasplantados renales. En estos individuos, la infección puede asociarse a la disfunción y pérdida del injerto renal. Objetivo: Describir el caso de una paciente con transplante renal, atendida en el Hospital Clínico de la Facultad de Medicina de Marília, que murió probablemente como resultado de complicaciones por una hemodiálisis después de la pérdida del injerto por toxicidad del tratamiento de su enfermedad. Caso clínico: Paciente de 22 años, residente en una región endémica para LVA, con inmunosupresión debido a trasplante renal, que evolucionó con pérdida del injerto después de sucesivas recidivas, tratamiento y profilaxis medicamentosa contra LVA. Con la interrupción de la terapia inmunosupresora y el retorno a la terapia dialítica, no se observaron formas amastigotes en la muestra de aspirado de médula ósea. Sin embargo, después de un año, evolucionó a muerte por accidente vascular encefálico resultante de comorbilidades. Conclusiones: Se describe un caso raro de sucesivas recidivas de AVL y la toma de decisiones médicas difíciles debido a la disyuntiva terapéutica entre el uso de medicamentos inmunosupresivos para mantener el injerto renal y el tratamiento antiparasitario. El control parasitológico se logró con la suspensión de la inmunosupresión, lo que demuestra la importancia de un sistema inmunocompetente y la adyuvancia de drogas específicas para el control de la enfermedad(AU)

An inter-organ neural circuit for appetite suppression.

Glucagon-like peptide-1 (GLP-1) is a signal peptide released from enteroendocrine cells of the lower intestine. GLP-1 exerts anorectic and antimotility actions that protect the body against nutrient malabsorption. However, little is known about how intestinal GLP-1 affects distant organs despite rapid enzymatic inactivation. We show that intestinal GLP-1 inhibits gastric emptying and eating via intestinofugal neurons, a subclass of myenteric neurons that project to abdominal sympathetic ganglia. Remarkably, cell-specific ablation of intestinofugal neurons eliminated intestinal GLP-1 effects, and their chemical activation functioned as a GLP-1 mimetic. GLP-1 sensing by intestinofugal neurons then engaged a sympatho-gastro-spinal-reticular-hypothalamic pathway that links abnormal stomach distension to craniofacial programs for food rejection. Within this pathway, cell-specific activation of discrete neuronal populations caused systemic GLP-1-like effects. These molecularly identified, delimited enteric circuits may be targeted to ameliorate the abdominal bloating and loss of appetite typical of gastric motility disorders.

Safety and efficacy of convalescent plasma for severe COVID-19: a randomized, single blinded, parallel, controlled clinical study.

BACKGROUND: Convalescent plasma (CP) has been widely used to treat COVID-19 and is under study. However, the variability in the current clinical trials has averted its wide use in the current pandemic. We aimed to evaluate the safety and efficacy of CP in severe coronavirus disease 2019 (COVID-19) in the early stages of the disease. METHODS: A randomized controlled clinical study was conducted on 101 patients admitted to the hospital with confirmed severe COVID-19. Most participants had less than 14 days from symptoms onset and less than seven days from hospitalization. Fifty patients were assigned to receive CP plus standard therapy (ST), and 51 were assigned to receive ST alone. Participants in the CP arm received two doses of 250 mL each, transfused 24 h apart. All transfused plasma was obtained from "super donors" that fulfilled the following criteria: titers of anti-SARS-CoV-2 S1 IgG ≥ 1:3200 and IgA ≥ 1:800 antibodies. The effect of transfused anti-IFN antibodies and the SARS-CoV-2 variants at the entry of the study on the overall CP efficacy was evaluated. The primary outcomes were the reduction in viral load and the increase in IgG and IgA antibodies at 28 days of follow-up. The per-protocol analysis included 91 patients. RESULTS: An early but transient increase in IgG anti-S1-SARS-CoV-2 antibody levels at day 4 post-transfusion was observed (Estimated difference [ED], - 1.36; 95% CI, - 2.33 to - 0.39; P = 0.04). However, CP was not associated with viral load reduction in any of the points evaluated. Analysis of secondary outcomes revealed that those patients in the CP arm disclosed a shorter time to discharge (ED adjusted for mortality, 3.1 days; 95% CI, 0.20 to 5.94; P = 0.0361) or a reduction of 2 points on the WHO scale when compared with the ST group (HR adjusted for mortality, 1.6; 95% CI, 1.03 to 2.5; P = 0.0376). There were no benefits from CP on the rates of intensive care unit admission (HR, 0.82; 95% CI, 0.35 to 1.9; P = 0.6399), mechanical ventilation (HR, 0.66; 95% CI, 0.25 to 1.7; P = 0.4039), or mortality (HR, 3.2; 95% CI, 0.64 to 16; P = 0.1584). Anti-IFN antibodies and SARS-CoV-2 variants did not influence these results. CONCLUSION: CP was not associated with viral load reduction, despite the early increase in IgG anti-SARS-CoV-2 antibodies. However, CP is safe and could be a therapeutic option to reduce the hospital length of stay. Trial registration NCT04332835.

Chronic pain precedes disrupted eating behavior in low-back pain patients.

Chronic pain is associated with anhedonia and decreased motivation. These behavioral alterations have been linked to alterations in the limbic brain and could explain the increased risk for obesity in pain patients. The mechanism of these behavioral changes and how they set in in relation to the development of chronic pain remain however poorly understood. Here we asked how eating behavior was affected in low-back pain patients before and after they transitioned to chronic pain, compared to patients whose pain subsided. Additionally, we assessed how the hedonic perception of fat-rich food, which is altered in chronic pain patients, related to the properties of the nucleus accumbens in this patients' population. We hypothesized that the accumbens would be directly implicated in the hedonic processing of fat-rich food in pain patients because of its well-established role in hedonic feeding and fat ingestion, and its emerging role in chronic pain. Accordingly, we used behavioral assays and structural brain imaging to test sub-acute back pain patients (SBP) and healthy control subjects at baseline and at approximately one-year follow-up. We also studied a sample of chronic low-back pain patients (CLBP) at one time point only. We found that SBP patients who recovered at follow-up (SBPr) and CLBP patients showed disrupted eating behaviors. In contrast, SBP patients who persisted in having pain at follow-up (SBPp) showed intact eating behavior. From a neurological standpoint, only SBPp and CLBP patients showed a strong and direct relationship between hedonic perception of fat-rich food and nucleus accumbens volume. This suggests that accumbens alterations observed in SBPp patients in previous works might protect them from hedonic eating disruptions during the early course of the illness. We conclude that disrupted eating behavior specifically sets in after pain chronification and is accompanied by structural changes in the nucleus accumbens.

Dissection and surgical approaches to the mouse jugular-nodose ganglia.

The jugular-nodose ganglia contain the sensory peripheral neurons of the vagus nerve, linking visceral organs to the medulla oblongata. Accessing these ganglia in smaller animals without damaging the vascular and neural structures may be challenging, as ganglionic fibers imbed deeply into the carotid sheath, and vagal parasympathetic fibers cross through the interior of the ganglia. We describe a practical protocol for locating and accessing the mouse jugular-nodose ganglia in vivo, including instructions for intraganglionic injections and postperfusion dissection. For complete details on the use and execution of this protocol, please refer to Han et al. (2018).

Listeriose em pacientes nefropatas imunossuprimidos - relato de dois casos / Listeriosis in patients immunosuppressed nephropaths - report of two cases

Contexto: A Listeria monocytogenes é um bacilo gram-positivo de baixa patogenicidade na população geral, mas importante causa de mortalidade por sepse e meningite em pacientes imunocomprometidos. Receptores de órgãos sólidos e candidatos em tratamento de dessensibilização são suscetíveis à infecção pela Listeria monocytogenes, embora sua apresentação clínica seja pouco reconhecida. Descrição dos casos: Paciente do sexo masculino, 43 anos, internado devido a rejeição aguda de enxerto pós-transplante renal, apresenta pico febril matutino e cefaleia. Paciente do sexo feminino, 59 anos, com doença renal crônica e em terapia de dessensibilização devido reatividade a painel antígeno leucocitário humano, busca pronto-socorro com febre, cefaleia e diarreia. A infecção por Listeria monocytogenes foi confirmada por hemocultura em ambos os casos. Discussão: A ocorrência de listeriose é esporádica e associada ao consumo de alimentos altamente contaminados, como laticínios, produtos frescos e carnes processadas. A redução da imunocompetência é o principal fator de risco para o desenvolvimento da doença em não gestantes, bem como para o aumento da mortalidade. O diagnóstico é estabelecido majoritariamente por hemocultura e o exame do líquido cefalorraquidiano é imprescindível para acessar o acometimento do sistema nervoso central, uma vez que os sinais meníngeos podem estar ausentes. O tratamento é realizado com beta-lactâmicos ou aminoglicosídeos. A ampicilina foi utilizada nos casos relatados e promoveu boa resposta clínica. Conclusão: Os profissionais devem atentar para a gravidade da infecção por Listeria monocytogenes e considerar sua ocorrência em pacientes imunocomprometidos, fornecendo orientações profiláticas a todos os candidatos a transplante de órgãos sólidos e tratamento empírico nos casos suspeitos.

Nausea and the Brain: The Chemoreceptor Trigger Zone Enters the Molecular Age.

Area postrema in brainstem has long been known to trigger emesis by detecting blood-borne toxins and pathogens. In this issue, Zhang and colleagues provide a single-cell molecular atlas of this region, opening new possibilities for harnessing its neurons in vivo.

uso probiótico no transtorno do espectro autista e na esquizofrenia: revisão narrativa da literatura / Probiotic use in autistic spectrum disorder and schizophrenia: narrative literature review

Introdução: devido à grande prevalência do transtorno do espectro autista (TEA) e da esquizofrenia e o caráter incapacitante dessas patologias, fez-se necessário o desenvolvimento de tratamentos cada vez mais eficientes e com menos efeitos adversos. Sendo a microbiota um regulador da inflamação e tendo esta um papel fundamental na gênese dos transtornos psiquiátricos, o uso de probióticos pode ser uma alternativa segura e com baixo custo para o tratamento complementar das doenças psiquiátricas. Objetivo: realizar uma revisão narrativa sobre a eficácia do uso de probióticos na redução de sintomas clínicos e gastrointestinais, assim como da segurança no tratamento do TEA e da esquizofrenia. Metodologia: revisão dos estudos em humanos que avaliaram os efeitos terapêuticos dos probióticos no TEA e esquizofrenia. Resultados: foram selecionados 13 estudos, sendo 8 sobre TEA e 5 sobre esquizofrenia, com total de 485 pacientes. As evidências apontam melhora dos sintomas gastrintestinais dos pacientes com TEA e esquizofrenia; entretanto, sem mudanças conclusivas dos sintomas psiquiátricos na esquizofrenia, associado a potencial benefício no TEA. Conclusão: essa revisão sugere que o uso de probióticos tem um potencial benefício nos sintomas comportamentais no TEA, associado à melhora dos sintomas gastrointestinais na esquizofrenia e TEA; entretanto, não se observou mudanças nos sintomas psiquiátricos da esquizofrenia.

Introduction: due to the high prevalence of autism spectrum disorder (ASD) and schizophrenia and the disabling nature of these pathologies, it has become necessary to develop increasingly efficient treatments with less adverse effects. As the microbiota is a regulator of inflammation and having a fundamental role in the genesis of psychiatric disorders, the use of probiotics may be a safe and low-cost alternative for the complementary treatment of psychiatric diseases. Objective: to perform a narrative review on the fficacy of probiotics use in reducing clinical and gastrointestinal symptoms, and adverse effects of the use of probiotics in the treatment of ASD and schizophrenia. Methodology: review of studies in humans that evaluated the therapeutic effects of probiotics on ASD and schizophrenia. Results: 13 studies were selected, 8 on TEA and 5 on schizophrenia, with a total of 485 patients. Evidence points to improvement in gastrointestinal symptoms in patients with ASD and schizophrenia; however, there were no conclusive changes in psychiatric symptoms in schizophrenia, associated with a potential benefit in ASD. Conclusion: This review suggests that the use of probiotics has a potential benefit in behavioral symptoms in ASD, associated with the improvement of gastrointestinal symptoms in schizophrenia and ASD; however, there were no changes in the psychiatric symptoms of schizophrenia.

Author Correction: Microbiota modulate sympathetic neurons via a gut-brain circuit.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Microbiota modulate sympathetic neurons via a gut-brain circuit.

Connections between the gut and brain monitor the intestinal tissue and its microbial and dietary content1, regulating both physiological intestinal functions such as nutrient absorption and motility2,3, and brain-wired feeding behaviour2. It is therefore plausible that circuits exist to detect gut microorganisms and relay this information to areas of the central nervous system that, in turn, regulate gut physiology4. Here we characterize the influence of the microbiota on enteric-associated neurons by combining gnotobiotic mouse models with transcriptomics, circuit-tracing methods and functional manipulations. We find that the gut microbiome modulates gut-extrinsic sympathetic neurons: microbiota depletion leads to increased expression of the neuronal transcription factor cFos, and colonization of germ-free mice with bacteria that produce short-chain fatty acids suppresses cFos expression in the gut sympathetic ganglia. Chemogenetic manipulations, translational profiling and anterograde tracing identify a subset of distal intestine-projecting vagal neurons that are positioned to have an afferent role in microbiota-mediated modulation of gut sympathetic neurons. Retrograde polysynaptic neuronal tracing from the intestinal wall identifies brainstem sensory nuclei that are activated during microbial depletion, as well as efferent sympathetic premotor glutamatergic neurons that regulate gastrointestinal transit. These results reveal microbiota-dependent control of gut-extrinsic sympathetic activation through a gut-brain circuit.

Impaired hypocretin/orexin system alters responses to salient stimuli in obese male mice.

The brain has evolved in an environment where food sources are scarce, and foraging for food is one of the major challenges for survival of the individual and species. Basic and clinical studies show that obesity or overnutrition leads to overwhelming changes in the brain in animals and humans. However, the exact mechanisms underlying the consequences of excessive energy intake are not well understood. Neurons expressing the neuropeptide hypocretin/orexin (Hcrt) in the lateral/perifonical hypothalamus (LH) are critical for homeostatic regulation, reward seeking, stress response, and cognitive functions. In this study, we examined adaptations in Hcrt cells regulating behavioral responses to salient stimuli in diet-induced obese mice. Our results demonstrated changes in primary cilia, synaptic transmission and plasticity, cellular responses to neurotransmitters necessary for reward seeking, and stress responses in Hcrt neurons from obese mice. Activities of neuronal networks in the LH and hippocampus were impaired as a result of decreased hypocretinergic function. The weakened Hcrt system decreased reward seeking while altering responses to acute stress (stress-coping strategy), which were reversed by selectively activating Hcrt cells with chemogenetics. Taken together, our data suggest that a deficiency in Hcrt signaling may be a common cause of behavioral changes (such as lowered arousal, weakened reward seeking, and altered stress response) in obese animals.

Functional Connectome Analyses Reveal the Human Olfactory Network Organization.

The olfactory system is uniquely heterogeneous, performing multifaceted functions (beyond basic sensory processing) across diverse, widely distributed neural substrates. While knowledge of human olfaction continues to grow, it remains unclear how the olfactory network is organized to serve this unique set of functions. Leveraging a large and high-quality resting-state functional magnetic resonance imaging (rs-fMRI) dataset of nearly 900 participants from the Human Connectome Project (HCP), we identified a human olfactory network encompassing cortical and subcortical regions across the temporal and frontal lobes. Highlighting its reliability and generalizability, the connectivity matrix of this olfactory network mapped closely onto that extracted from an independent rs-fMRI dataset. Graph theoretical analysis further explicated the organizational principles of the network. The olfactory network exhibits a modular composition of three (i.e., the sensory, limbic, and frontal) subnetworks and demonstrates strong small-world properties, high in both global integration and local segregation (i.e., circuit specialization). This network organization thus ensures the segregation of local circuits, which are nonetheless integrated via connecting hubs [i.e., amygdala (AMY) and anterior insula (INSa)], thereby enabling the specialized, yet integrative, functions of olfaction. In particular, the degree of local segregation positively predicted olfactory discrimination performance in the independent sample, which we infer as a functional advantage of the network organization. In sum, an olfactory functional network has been identified through the large HCP dataset, affording a representative template of the human olfactory functional neuroanatomy. Importantly, the topological analysis of the olfactory network provides network-level insights into the remarkable functional specialization and spatial segregation of the olfactory system.

Rethinking Food Reward.

The conscious perception of the hedonic sensory properties of caloric foods is commonly believed to guide our dietary choices. Current and traditional models implicate the consciously perceived hedonic qualities of food as driving overeating, whereas subliminal signals arising from the gut would curb our uncontrolled desire for calories. Here we review recent animal and human studies that support a markedly different model for food reward. These findings reveal in particular the existence of subcortical body-to-brain neural pathways linking gastrointestinal nutrient sensors to the brain's reward regions. Unexpectedly, consciously perceptible hedonic qualities appear to play a less relevant, and mostly transient, role in food reinforcement. In this model, gut-brain reward pathways bypass cranial taste and aroma sensory receptors and the cortical networks that give rise to flavor perception. They instead reinforce behaviors independently of the cognitive processes that support overt insights into the nature of our dietary decisions.

On the roles of the Duodenum and the Vagus nerve in learned nutrient preferences.

BACKGROUND AND AIM: In most species, including humans, food preference is primarily controlled by nutrient value. However, the gut-brain pathways involved in preference learning remain elusive. The aim of the present study, performed in C57BL6/J mice, was to characterize the roles in nutrient preference of two critical elements of gut-brain pathways, i.e. the duodenum and vagal gut innervation. METHODS: Adult wild-type C57BL6/J mice from a normal-weight cohort sustained one of the following three procedures: duodenal-jejunal bypass intestinal rerouting (DJB), total subdiaphragmatic vagotomy (SDV), or sham surgery. Mice were assessed in short-term two-bottle preference tests before and after 24 h s exposures to solutions containing one of glutamate, lipids, sodium, or glucose. RESULTS: DJB and SDV interfered in preference formation in a nutrient-specific manner: whereas normal preference learning for lipids and glutamate was disrupted by both DJB and SDV, these interventions did not alter the formation of preferences for glucose. Interestingly, sodium preferences were abrogated by DJB but not by SDV. CONCLUSIONS: Different macronutrients make use of distinct gut-brain pathways to influence food preferences, thereby mirroring nutrient-specific processes of food digestion. Specifically, whereas both vagal innervation and duodenal sensing appear critical for generating responses to fats and protein, glucose preferences recruit post-duodenal, vagal-independent pathways in pair with the control of glucose homeostasis. Overall, our data suggest that the physiological processes involved in digesting and absorbing fats, amino acids, and glucose overlap with those mediating learned preferences for each of these nutrients.

Postpartum Depression: Epidemiological Clinical Profile of Patients Attended In a Reference Public Maternity in Salvador-BA.

OBJECTIVE: To evaluate the clinical epidemiological state of women with suspected postpartum depression (PPD) in a public maternity hospital in Salvador, state of Bahia, Brazil. METHODS: A cross-sectional research was performed with puerperal patients attended at a public maternity hospital in Salvador, Bahia. Data collection was performed from June to September 2017. The Edinburgh Postnatal Depression Scale was used as a screening instrument, and, subsequently, women with positive scores answered a questionnaire to identify their clinical and epidemiological status. RESULTS: Out of 151 postpartum women from the research, 30 (19.8%) presented suspicion of PPD. There was a prevalence of single mothers 13 (43.3%), women with complete fundamental education 15 (50.0%), women with black skin color 14 (46.7%), and those with a monthly family income of up to one minimum wage 18 (40.0%). CONCLUSION: Although PPD is an underdiagnosed disease, a high prevalence of the condition was found in our research. It is, then, considered that these results reinforce its significance as a public health problem, requiring prevention strategies, early diagnosis and effective treatment.

OBJETIVO: Avaliar o perfil clínico epidemiológico de mulheres com suspeita de Depressão Pós-Parto em uma maternidade pública de referência de Salvador, no estado da BA. MéTODOS: Estudo transversal, realizado com puérperas atendidas em uma maternidade pública de referência de Salvador, BA. A coleta de dados foi realizada de junho até setembro de 2017. Utilizou-sea escala de Edimburgo como instrumento, e, posteriormente, as mulheres com escore positivo responderam a um questionário para a identificação do seu perfil clínico e epidemiológico. RESULTADOS: Das 151 puérperas pesquisadas, 30 (19,8%) apresentaram suspeita de depressão pós-parto. Predominaram as puérperas solteiras 13 (43,3%), com ensino médio completo 15 (50,0%), cor da pele preta 14 (46,7%), e aquelas com renda familiar mensal de até um salário mínimo 18 (40,0%). CONCLUSãO: Ainda que a depressão pós-parto seja uma enfermidade subdiagnosticada, neste estudo verificou-se uma elevada prevalência da condição. Considera-se, então que estes resultados reforçam o seu significado como problema de saúde pública, exigindo estratégias de prevenção, diagnóstico precoce e tratamento efetivo.

Postpartum depression: epidemiological clinical profile of patients attended in a reference public maternity in Salvador-BA / Depressão pós-parto: perfil clínico epidemiológico de pacientes atendidas em uma maternidade pública de referência em Salvador-BA

Abstract Objective To evaluate the clinical epidemiological state of women with suspected post partum depression (PPD) in a public maternity hospital in Salvador, state of Bahia, Brazil. Methods A cross-sectional research was performed with puerperal patients attended at a public maternity hospital in Salvador, Bahia. Data collection was performed from June to September 2017. The Edinburgh Postnatal Depression Scale was used as a screening instrument, and, subsequently, women with positive scores answered a questionnaire to identify their clinical and epidemiological status. Results Out of 151 postpartum women from the research, 30 (19.8%) presented suspicion of PPD. There was a prevalence of single mothers 13 (43.3%), women with complete fundamental education 15 (50.0%), women with black skin color 14 (46.7%), and those with a monthly family income of up to one minimum wage 18 (40.0%). Conclusion Although PPD is an underdiagnosed disease, a high prevalence of the condition was found in our research. It is, then, considered that these results reinforce its significance as a public health problem, requiring prevention strategies, early diagnosis and effective treatment.

Resumo Objetivo Avaliar o perfil clínico epidemiológico de mulheres com suspeita de Depressão Pós-Parto em uma maternidade pública de referência de Salvador, no estado da BA. Métodos Estudo transversal, realizado com puérperas atendidas em uma maternidade pública de referência de Salvador, BA. A coleta de dados foi realizada de junho até setembro de 2017. Utilizou-sea escala de Edimburgo como instrumento, e, posteriormente, as mulheres com escore positivo responderam a um questionário para a identificação do seu perfil clínico e epidemiológico. Resultados Das 151 puérperas pesquisadas, 30 (19,8%) apresentaram suspeita de depressão pós-parto. Predominaram as puérperas solteiras 13 (43,3%), com ensino médio completo 15 (50,0%), cor da pele preta 14 (46,7%), e aquelas com renda familiar mensal de até um salário mínimo 18 (40,0%). Conclusão Ainda que a depressão pós-parto seja uma enfermidade subdiagnosticada, neste estudo verificou-se uma elevada prevalência da condição. Considera-se, então que estes resultados reforçam o seu significado como problema de saúde pública, exigindo estratégias de prevenção, diagnóstico precoce e tratamento efetivo.