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Relapsing polychondritis is a rare multisystem disease involving cartilaginous and proteoglycan-rich structures. The diagnosis of this disease is mainly suggested by the presence of flares of inflammation of the cartilage, particularly in the ears, nose or respiratory tract, and more rarely, in the presence of other manifestations. The spectrum of clinical presentations may vary from intermittent episodes of painful and often disfiguring auricular and nasal chondritis to an occasional organ or even life-threatening manifestations such as lower airway collapse. There is a lack of awareness about this disease is mainly due to its rarity. In 2020, VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome, a novel autoinflammatory syndrome, was described. VEXAS syndrome is attributed to somatic mutations in methionine-41 of UBA1, the major E1 enzyme that initiates ubiquitylation. This new disease entity connects seemingly unrelated conditions: systemic inflammatory syndromes (relapsing chondritis, Sweet's syndrome, and neutrophilic dermatosis) and hematologic disorders (myelodysplastic syndrome or multiple myeloma). Therefore, this article reviews the current literature on both disease entities.

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Acute kidney injury (AKI) often triggers physiological processes aimed at restoring renal function and architecture. However, this response can become maladaptive, leading to nephron loss and fibrosis. Although the therapeutic effects of resveratrol (RSV) are well established, its impact after AKI and for subsequent chronic kidney disease (CKD) remains unclear. This study assessed whether transient administration of RSV following ischaemia-reperfusion injury (IRI) could prevent the progression to CKD. Forty-one male Wistar rats were assigned randomly to sham surgery, bilateral renal ischaemia for 30 min (IR) or IR+RSV. The RSV treatment commenced 24 h after IRI and continued for 10 days. The rats were studied for either 10 days or 5 months, after which kidney function and structure were evaluated. Mitochondrial homeostasis, oxidant defence and renal inflammation state were also evaluated. Despite having the same severity of AKI, rats receiving RSV for 10 days after IRI exhibited significant improvement in kidney histological injury and reduced inflammation, although renal haemodynamic recovery was less pronounced. Resveratrol effectively prevented the elevation of tubular injury-related molecules and profibrotic signalling with reduced myofibroblast proliferation. Furthermore, RSV substantially improved the antioxidant response and mitochondrial homeostasis. After 5 months, RSV prevented the transition to CKD, as evidenced by the prevention of progressive proteinuria, renal dysfunction and tubulointerstitial fibrosis. This study demonstrates that a brief treatment with RSV following IRI is enough to prevent maladaptive repair and the development of CKD. Our findings highlight the importance of the early days of reperfusion, indicating that maladaptive responses can be reduced effectively following severe AKI. KEY POINTS: Physiological processes activated after acute kidney injury (AKI) can lead to maladaptive responses, causing nephron loss and fibrosis. Prophylactic renoprotection with resveratrol (RSV) has been described in experimental AKI, but its impact after AKI and for subsequent chronic kidney disease (CKD) remains unclear. In this study, we found that histological tubular injury persists 10 days after ischaemia-reperfusion injury and contributes to a failed repair phenotype in proximal tubular cells. Short-term RSV intervention influenced the post-ischaemic repair response and accelerated tubular recovery by reducing oxidative stress and mitochondrial damage. Furthermore, RSV targeted inflammation and profibrotic signalling during the maladaptive response, normalizing both processes. Resveratrol effectively prevented AKI-to-CKD transition even 5 months after the intervention. The study serves as a proof of concept, proposing RSV as a valuable candidate for further translational clinical studies to mitigate AKI-to-CKD transition.

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El síndrome de Brown-Séquard es el conjunto de signos y síntomas causado por hemisección medular de diversos orígenes. Puede generarse por múltiples causas; las traumáticas son las más frecuentes. Las causas menos frecuentes son patología inflamatoria, isquémica, tumoral o infecciosa. Se presenta un niño de 12 años, con instauración aguda y progresiva de un síndrome de hemisección medular derecho, con parálisis hipo/arrefléctica homolateral y afectación de sensibilidad termoalgésica contralateral. En la resonancia magnética de médula espinal, se observó compromiso inflamatorio en hemimédula derecha a nivel de segunda y tercera vértebras torácicas. Con diagnóstico de mielitis transversa idiopática, inició tratamiento con corticoide intravenoso a altas dosis con evolución clínica favorable y restitución de las funciones neurológicas.

Brown-Séquard syndrome refers to a set of signs and symptoms caused by hemisection of the spinal cord from various sources. It may have multiple causes; traumatic injuries are the most frequent ones. The less common causes include inflammation, ischemia, tumors, or infections. This report is about a 12-year-old boy with an acute and progressive course of right hemisection of the spinal cord, with ipsilateral hypo/areflexic paralysis and contralateral loss of thermalgesic sensation. The MRI of the spinal cord showed inflammation in the right side of the spinal cord at the level of the second and third thoracic vertebrae. The patient was diagnosed with idiopathic transverse myelitis and was started on intravenous high-dose corticosteroids; he showed a favorable clinical course and recovered neurological functions.

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Asthma is one of the most common chronic non-communicable diseases worldwide, characterized by variable airflow limitation secondary to airway narrowing, airway wall thickening, and increased mucus resulting from chronic inflammation and airway remodeling. Current epidemiological studies reported that hypovitaminosis D is frequent in patients with asthma and is associated with worsening the disease and that supplementation with vitamin D3 improves asthma symptoms. However, despite several advances in the field, the molecular mechanisms of asthma have yet to be comprehensively understood. MicroRNAs play an important role in controlling several biological processes and their deregulation is implicated in diverse diseases, including asthma. Evidence supports that the dysregulation of miR-21, miR-27b, miR-145, miR-146a, and miR-155 leads to disbalance of Th1/Th2 cells, inflammation, and airway remodeling, resulting in exacerbation of asthma. This review addresses how these molecular mechanisms explain the development of asthma and its exacerbation and how vitamin D3 may modulate these microRNAs to improve asthma symptoms.

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BACKGROUND: Obesity impairs homeostatic control of energy and is associated with chronic low-grade inflammation. Effects of glucagon-like peptide-1, the target in the gastrointestinal tract for anti-obesity drugs such as Liraglutide, were not properly associated with inflammation markers. This study investigated the effects of Liraglutide on metabolic and gastrointestinal parameters in a rat model of obesity. METHODS: Twenty-six Wistar rats with obesity were randomly distributed to receive saline (n = 10), 400 µg (n = 8), or 1200 µg of Liraglutide/kg/day (n = 8), subcutaneously for 30 consecutive days, once a day. Weight gain, feeding efficiency, caloric consumption, gastric motility, adiposity, histomorphometric, murinometric, biochemical parameters and cytokines TNF-α and TGF-ß1 in duodenal tissue were measured. Data were analysed by ANOVA, followed by Bonferroni post hoc or Kruskal-Wallis test, followed by Dunn's multiple comparison test. RESULTS: Liraglutide-treated animals had better feeding efficiency and higher caloric intake in a dose-dependent manner. Higher doses slowed gastric emptying and diminished the amplitude of gastric contractions. These effects were accompanied by decreases in intestinal muscle layer thickness and crypt depth. Liraglutide significantly reduced retroperitoneal and visceral white adipose tissue depots. High-dose treatment decreased levels of TNF-α and enhanced levels of TGF-ß1 in duodenal tissue. Liraglutide treatment provided significant reductions in total cholesterol, triglyceride and hepatic transaminases. CONCLUSIONS: Liraglutide reduced fat accumulation, improved metabolic parameters and downregulated levels of inflammatory signalling in duodenal tissue. Liraglutide at high doses controlled obesity-related outcomes, and such effects seemed to be driven by its action on glucagon-like peptide-1 receptors in the gastrointestinal tract slowing gastric motility.

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Brown-Séquard syndrome refers to a set of signs and symptoms caused by hemisection of the spinal cord from various sources. It may have multiple causes; traumatic injuries are the most frequent ones. The less common causes include inflammation, ischemia, tumors, or infections. This report is about a 12-year-old boy with an acute and progressive course of right hemisection of the spinal cord, with ipsilateral hypo/areflexic paralysis and contralateral loss of thermalgesic sensation. The MRI of the spinal cord showed inflammation in the right side of the spinal cord at the level of the second and third thoracic vertebrae. The patient was diagnosed with idiopathic transverse myelitis and was started on intravenous high-dose corticosteroids; he showed a favorable clinical course and recovered neurological functions.

El síndrome de Brown-Séquard es el conjunto de signos y síntomas causado por hemisección medular de diversos orígenes. Puede generarse por múltiples causas; las traumáticas son las más frecuentes. Las causas menos frecuentes son patología inflamatoria, isquémica, tumoral o infecciosa. Se presenta un niño de 12 años, con instauración aguda y progresiva de un síndrome de hemisección medular derecho, con parálisis hipo/arrefléctica homolateral y afectación de sensibilidad termoalgésica contralateral. En la resonancia magnética de médula espinal, se observó compromiso inflamatorio en hemimédula derecha a nivel de segunda y tercera vértebras torácicas. Con diagnóstico de mielitis transversa idiopática, inició tratamiento con corticoide intravenoso a altas dosis con evolución clínica favorable y restitución de las funciones neurológicas.

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Zika virus (ZIKV) is a mosquito-borne virus first reported from humans in Nigeria in 1954. The first outbreak occurred in Micronesia followed by an outbreak in French Polynesia and another in Brazil when the virus was associated with numerous cases of severe neurological manifestations such as Guillain-Barre syndrome in adults and congenital zika syndrome in fetuses, particularly congenital microcephaly. Innate immunity is the first line of defense against ZIKV through triggering an antiviral immune response. Along with innate immune responses, a sufficient balance between anti- and pro-inflammatory cytokines and the amount of these cytokines are triggered to enhance the antiviral responses. Here, we reviewed the complex interplay between the mediators and signal pathways that coordinate antiviral immune response and inflammation as a key to understanding the development of the underlying diseases triggered by ZIKV. In addition, we summarize current and new therapeutic strategies for ZIKV infection, highlighting cardiotonic steroids as antiviral drugs for the development of this agent.

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Parkinson's Disease (PD) is characterized by classic motor symptoms related to movement, but PD patients can experience symptoms associated with impaired autonomic function, such as respiratory disturbances. Functional respiratory deficits are known to be associated with brainstem neurodegeneration in the mice model of PD induced by 6-hydroxydopamine (6-OHDA). Understanding the causes of neuronal death is essential for identifying specific targets to prevent degeneration. Many mechanisms can explain why neurons die in PD, and neuroinflammation is one of them. To test the influence of inflammation, mediated by microglia and astrocytes cells, in the respiratory disturbances associated with brainstem neurons death, we submitted wild-type (WT) and TNF receptor 1 (TNFR1) knockout male mice to the 6-OHDA model of PD. Also, male C57BL/6 animals were induced using the same PD model and treated with minocycline (45 mg/kg), a tetracycline antibiotic with anti-inflammatory properties. We show that degeneration of brainstem areas such as the retrotrapezoid nucleus (RTN) and the pre-Botzinger Complex (preBotC) were prevented in both protocols. Notably, respiratory disturbances were no longer observed in the animals where inflammation was suppressed. Thus, the data demonstrate that inflammation is responsible for the breathing impairment in the 6-OHDA-induced PD mouse model.

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Concentrações aumentadas de tecido adiposo corporal observadas no sobrepeso e obesidade, podem gerar a produção de diversos mediadores inflamatórios com ação direta ou indireta em influenciar a capacidade de proliferação e diferenciação das células hematopoéticas e, consequentemente, a complexa regulação que envolve os processos de migração celular. Sabe-se que o recrutamento contínuo de leucócitos durante vários estágios do processo inflamatório apresenta importante papel na gênese desse processo, participando intensamente na perpetuação da inflamação. Na literatura, vários estudos demostraram acapacidade anti-inflamatória das antocianinas sobre vários órgãos; contudo poucos estudos avaliam a influência das antocianinas sobre a migração celular. As antocianinas pertencem à ampla classe dos flavonoides que estão presentes em uma ampla variedade de frutas, vegetais e bebidas e são os compostos responsáveis pelas cores azul, violeta e vermelha desses alimentos. Sendo assim, pretende-se nesse estudo avaliar o efeito da delfinidina-3-glicosídeo, uma antocianina presente em abundância em diversas frutas com destaque para o suco de uva integral, sobre os processos de migração leucocitária. Para tanto esse trabalho foi dividido em duas etapas: (i) uma realizada em pacientes com sobrepeso que consumiram suco de uva integral e (ii) uma segunda etapa, in vitro, onde foi avaliado o efeito da delfinidina-3-glicosídeo sobre mecanismos envolvidos na modulação dos processos de migração leucocitária. Na etapa inicial com estudos in vivo, foram avaliados parâmetros bioquímicos, hematológicos, bem como a expressão de moléculas de adesão de células polimorfonucleares do sangue periférico e a quantificação de citocinas inflamatórias e alguns genes envolvidos nos processos de inflamação e migração celular. Na primeira etapa, a ingestão de suco de uva não alterou o perfil lipídico/inflamatório ou a contagem de leucócitos, entretanto, reduziu os valores circulantes de sICAM e sVCAM. Na segunda etapa, os resultados in vitro mostraram que a delfinidina reduziu a taxa de migração e a expressão de células CD11/CD18 positivas, reduziu a expressão gênica de ICAM-1 e a fosforilação e expressão gênica de NFkB, reduzindo também a produção de IL-6, IL-8 e CCL2

Increased concentrations of body adipose tissue observed in overweight and obesity may generate the production of several inflammatory mediators that can act directly or indirectly on the hematopoietic cells capacity of proliferation and differentiation and, consequently, the complex regulation that involves the processes of cell migration. It is known that the continuous recruitment of leukocytes during various stages of the inflammatory process plays an important role in the genesis of this process, intensely participating in the perpetuation of inflammation. In the literature, several studies have demonstrated the anti-inflammatory capacity of anthocyanins on various organs; however, few studies have evaluated the influence of anthocyanins on cell migration. Anthocyanins belong to the broad class of flavonoids that are present in a wide variety of fruits, vegetables and beverages and are the compounds responsible for the blue, violet and red colors of these foods. Thus, this study intends to evaluate the effect of delphinidin-3-glycoside, an anthocyanin present in abundance in several fruits, especially whole grape juice, on leukocyte migration processes. Therefore, this study was divided into two stages: (i) one performed in overweight patients who consumed whole grape juice and (ii) a second stage, in vitro, where the effect of delphinidin-3-glycoside on mechanisms involved in the modulation of leukocyte migration processes was evaluated. In the initial stage with in vivo studies, biochemical and hematological parameters were evaluated, as well as the expression of adhesion molecules of polymorphonuclear cells of peripheral blood and the quantification of inflammatory cytokines and some genes involved in the processes of inflammation and cell migration. In the first stage, the intake of grape juice did not alter the lipid/inflammatory profile or the leukocyte count, however, it reduced the circulating values of sICAM and sVCAM. In the second step, in vitro results showed that delphinidine reduced the migration rate and expression of CD11/CD18 positive cells, reduced ICAM-1 gene expression and NFkB phosphorylation and gene expression, and also reduced IL-6, IL-8 and CCL2 production

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Obesity is associated with inflammation and an increased risk of cardiovascular disease and premature mortality, as well as a range of other conditions. Obesity is a growing global problem, not only in adults, but also in children and adolescents. Therefore, the present study aimed to assess the effects of a one-year interdisciplinary intervention on the cardiometabolic and inflammatory profiles of adolescents with obesity. Twenty-two adolescents completed the intervention, which included clinical, nutritional, psychological and physical exercise counselling. Body composition, and metabolic, inflammatory, and cardiovascular risk biomarkers were analyzed before and after one year of intervention. Visceral and subcutaneous fat were determined ultrasonographically. The homeostasis model assessment of insulin resistance (HOMA-IR) and the quantitative insulin sensitivity check index (QUICKI) equation were used to estimate insulin resistance and insulin sensitivity, respectively. A reduction in body mass, adiposity, glucose, and insulin and an improved lipid profile were observed after the therapy. Hyperleptinemia was reduced from 77.3% to 36.4%. Plasminogen activator inhibitor-1 (PAI-1), intercellular adhesion molecule 1 (ICAM-1), leptin, the leptin/adiponectin ratio, and the adiponectin/leptin ratio were also significantly improved. Metabolic changes were associated with a reduction in visceral fat and waist circumference, and adiponectin and the leptin/adiponectin ratio were associated with HOMA-IR. The interdisciplinary therapy promoted improvements in hyperleptinemia and metabolic, inflammatory, and cardiovascular biomarkers.

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The rising fructose intake in sugar-sweetened beverages and ultra-processed foods relates to the high incidence of nonalcoholic fatty liver disease. This study aimed to examine the effects of long-term high-fructose diet intake (for 16 or 20 weeks) on progressive hepatic damage, focusing on the endoplasmic reticulum stress markers and fibrogenesis as possible triggers of liver fibrosis. Forty 3-month-old male C57BL/6J mice were randomly divided into four nutritional groups: C16 (control diet for 16 weeks), C20 (control diet for 20 weeks), HFRU16 (high-fructose diet for 16 weeks), and HFRU20 (high-fructose diet for 20 weeks). Both HFRU groups showed oral glucose intolerance and insulin resistance, but only the HFRU20 group exhibited increased inflammation. The increased lipogenic and endoplasmic reticulum stress markers triggered hepatic fibrogenesis. Hence, time-dependent perivascular fibrosis with positive immunostaining for alpha-smooth muscle actin and reelin in HFRU mice was observed, ensuring fibrosis development in this mouse model. Our study showed time-dependent and progressive damage on hepatic cytoarchitecture, with maximization of hepatic steatosis without overweight in HFRU20 mice. ER stress and liver inflammation could mediate hepatic stellate cell activation and fibrogenesis, emerging as targets to prevent NAFLD progression and fibrosis onset in this dietary model.

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Obesity and depression, disorders associated with inflammation, have high incidences in women. Understanding the derangements present in the initial phase of obesity may point to factors that could help avoiding disease aggravation. The present study aimed at investigating the effects of a 6-months interdisciplinary therapy for weight loss in women with grade I obesity. Before and after the therapy, 37 middle-aged women donated blood and responded to questionnaires for depression and anxiety symptoms. Inflammatory parameters were evaluated in serum and a preliminary screening of the plasma proteome was performed. The therapy decreased anthropometric, psychological scores, and serum levels of inflammatory parameters. Depression and anxiety scores correlated positively with some inflammatory parameters. The proteomic analysis showed changes in proteins related to cholesterol metabolism and inflammatory response. Interdisciplinary therapy improves anthropometric and inflammatory statuses and ameliorating psychological symptoms. The decrease of MCP-1 levels after interdisciplinary therapy has not been reported so far, at the best of our knowledge. The present demonstration of positive associations of inflammatory markers and psychological scores indicate that these mediators may be useful to monitor psychological status in obesity. The present proteome data, although preliminary, pointed to plasma alterations indicative of improvement of inflammation after interdisciplinary therapy.

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BACKGROUND AND AIMS: Non-alcoholic fatty liver disease (NAFLD) is a multisystem disease closely linked to cardiovascular disease (CVD). This study aims to investigate the connection between early-stage NAFLD and atherosclerosis, as well as the correlation between liver fibrosis and coronary heart disease while exploring underlying inflammatory mechanisms. METHODS: In this retrospective study, the authors analyzed data from 607 patients who underwent both coronary computed tomography angiography (CCTA) and abdominal ultrasonography (US). Logistic regression was utilized to examine the association between NAFLD and atherosclerosis, while mediation analysis was conducted to explore whether inflammatory markers mediate the link between liver fibrosis and coronary artery disease. RESULTS: Among the 607 patients included, 237 (39.0 %) were diagnosed with NAFLD through ultrasonography. After adjusting for traditional cardiovascular risk factors, ALT, and AST, NAFLD demonstrated a significant correlation with carotid intimal thickening (1.58, 95 % CI 1.04‒2.40; p = 0.034) and non-calcified plaque (1.56, 95 % CI 1.03‒2.37; p = 0.038). Additionally, fibrosis predictive markers, including FIB-4 > 1.3 (1.06, 95 % CI 2.30‒5.00; p = 0.035) and APRI (6.26, 95 % CI 1.03‒37.05; p = 0.046), independently correlated with coronary heart disease after adjusting for cardiovascular risk factors. Conversely, among systemic inflammatory markers, only the neutrophil-to-lymphocyte ratio (NLR) and systemic inflammatory response index (SIRI) are independently associated with coronary heart disease. ROC curve analysis indicated that combining predictive fibrosis markers or inflammatory markers with traditional cardiovascular risk factors enhanced the predictive accuracy for coronary heart disease. Mediation analysis revealed that NLR fully mediated the effect of liver fibrosis on coronary heart disease. CONCLUSION: NAFLD is associated with carotid intimal thickening and non-calcified plaque, suggesting an increased cardiovascular risk. Furthermore, liver fibrosis independently increases the risk of coronary heart disease in the early-stage NAFLD population, and inflammation may play a fully mediating role in the effect of liver fibrosis on coronary heart disease. Early intervention is crucial for NAFLD patients to mitigate future major adverse cardiovascular events.

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BACKGROUND: Near-infrared irradiation photobiomodulation (NIR-PBM) has been successfully used in periodontal treatment as an adjuvant tool to locally improve cell function and regeneration. Although the relationship between periodontitis and systemic disease constitutes an important aspect of periodontal clinical research, the systemic effects of NIR-PBM in periodontitis are not well known. In this study, we aimed to investigate the effects of NIR-PBM on systemic oxidative stress and inflammation in an apolipoprotein E (ApoE) knockout mouse model of periodontal disease (PD). METHODS: We evaluated alveolar bone loss by measuring the distance from the cementoenamel junction (CEJ) to the alveolar bone crest (ABC), reactive oxygen species (ROS) production in blood cells, inflammatory activity, plasma cholesterol levels, and lipid peroxidation levels in three experimental groups: (1) ApoEC, control group without intervention; (2) ApoEP, first molar ligation-induced periodontitis for 4 weeks; and (3) ApoEP + PBM, exposed to 808 nm continuous wave, ø ~ 3 mm2, 100 mW, 60 s of NIR-PBM for 7 consecutive days after 4 weeks of periodontitis. At the end of the experimental protocols, ApoEP mice presented significantly increased alveolar bone loss, ROS production, inflammatory activity, plasma cholesterol, and lipid peroxidation levels compared to the ApoEC group (P < 0.05). NIR-PBM for 7 days in the ApoEP + PBM mice significantly decreased systemic ROS production, inflammatory response, plasma cholesterol, and lipid peroxidation levels, similar to those found in the ApoEC group (P > 0.05). However, it was not capable of preventing alveolar bone loss (P > 0.05 compared to ApoEP mice). CONCLUSION: A 7-day treatment with NIR-PBM effectively reduces systemic oxidative stress and inflammatory parameters in hypercholesterolemic mice with PD. However, more studies with longer evaluation times are needed to confirm the systemic effects of locally applied NIR-PBM on PD associated with hypercholesterolemia.

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BACKGROUND: Varicocele is one of the main causes of male infertility. Although the pathophysiology mechanism of varicocele is very well described and understood, there are some unanswered questions that remains unknown. Some studies have previously described the state of testicular inflammation and sperm in animal models, especially the mouse model, and the seminal plasma of men with varicocele, with or without changes in semen parameters. METHODS OF STUDY: This review intended to verify the role of inflammatory mechanism in varicocele, using clinical studies as well as animal model studies on the effect of inflammation caused by varicocele on the function of testicular somatic and germ cells. RESULTS: In-vivo studies confirmed whether anti-inflammatory molecules could treat the semen of men with varicocele and rats with varicocele. The use of different anti-inflammatory agents in mouse model studies provided a new perspective for future clinical studies to investigate the effect of concurrent treatment with surgery to improve surgical outcomes. CONCLUSION: Similar to animal model studies, previously conducted clinical trials have demonstrated the effectiveness of anti-inflammatory therapy in varicocele patients. However, clinical trials using anti-inflammatory are needed to be conducted agents to evaluate different aspects of this therapeutical approach in varicocele patients.

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Chronic consumption of hyperpalatable and hypercaloric foods has been pointed out as a factor associated with cognitive decline and memory impairment in obesity. In this context, the integration between peripheral and central inflammation may play a significant role in the negative effects of an obesogenic environment on memory. However, little is known about how obesity-related peripheral inflammation affects specific neurotransmission systems involved with memory regulation. Here, we test the hypothesis that chronic exposure to a highly palatable diet may cause neuroinflammation, glutamatergic dysfunction, and memory impairment. For that, we exposed C57BL/6J mice to a high sugar and butter diet (HSB) for 12 weeks, and we investigated its effects on behavior, glial reactivity, blood-brain barrier permeability, pro-inflammatory features, glutamatergic alterations, plasticity, and fractalkine-CX3CR1 axis. Our results revealed that HSB diet induced a decrease in memory reconsolidation and extinction, as well as an increase in hippocampal glutamate levels. Although our data indicated a peripheral pro-inflammatory profile, we did not observe hippocampal neuroinflammatory features. Furthermore, we also observed that the HSB diet increased hippocampal fractalkine levels, a key chemokine associated with neuroprotection and inflammatory regulation. Then, we hypothesized that the elevation on glutamate levels may saturate synaptic communication, partially limiting plasticity, whereas fractalkine levels increase as a strategy to decrease glutamatergic damage.

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OBJECTIVE: Compare erythropoiesis-related factors between different stages of canine chronic kidney disease (CKD). ANIMALS: 8 healthy adult dogs (controls), and 24 dogs with CKD, equally divided into 3 groups based on International Renal Interest Society-CKD Guidelines (stage 2, 3, and 4) were recruited between December 2012 and December 2014. METHODS: The following were assessed in all dogs and then compared between groups: bone marrow cytology, CBC, reticulocyte count, urinalysis, serum biochemistry, blood pressure, occult gastrointestinal bleeding, and serum concentrations of parathyroid hormone (PTH), erythropoietin, interleukin-1ß, interleukin-3, tumor necrosis factor-α (TNFα), and interferon-γ. RESULTS: Erythropoiesis inducing and suppressing factors and the results of the bone marrow cytology of dogs in stage 2 CKD did not differ from the control group. The presence of reticulocytosis in CKD stage 2 suggests that blood loss or erythrocyte destruction might be contributing to developing anemia. Anemia in dogs with progressive CKD was associated with increasing PTH and TNFα and with elevation of the ratio of myeloid to erythroid precursor cells caused by hypoplasia of the erythroid series. The latter was represented mainly by a decrease in the population of polychromatophilic rubricytes and metarubricytes. CLINICAL RELEVANCE: Increased PTH and TNFα seem to contribute to the reduced percentage of polychromatophilic rubricytes and erythroid population, thereby aggravating the anemia of dogs with advanced CKD. Gastrointestinal blood loss contributes to anemia in all canine CKD stages.

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BACKGROUND: Few studies have evaluated the association between diet-related inflammation and gastric adenocarcinoma (GA) and evidence is scarce in Brazil. This study evaluated the association between a pro-inflammatory diet and GA. METHODS: A multicenter case-control study was conducted in Brazil. A total of 1645 participants-492 cases, 377 endoscopy controls, and 776 hospital controls-were included. Energy-adjusted Dietary Inflammatory Index (E-DIITM) scores were derived from a validated food frequency questionnaire. We used binary and multinomial logistic regression models for the analysis of total GA, and its subtypes (cardia and non-cardia, intestinal, and diffuse histological subtypes). RESULTS: In cases versus endoscopy controls, a pro-inflammatory diet, estimated by higher E-DII scores, was associated with a higher risk GA (ORQ4vsQ1: 2.60, 1.16-5.70), of non-cardia GA (OR: 2.90, 1.06-7.82), and diffuse subtype (OR: 3.93, 1.59-9.70). In cases versus hospital controls, higher E-DII scores were associated with a higher risk of GA (OR: 2.70, 1.60-4.54), of cardia GA (OR: 3.31, 1.32-8.24), non-cardia GA (OR: 2.97, 1.64-5.39), and both intestinal (OR: 2.82, 1.38-5.74) and diffuse GA (OR: 2.50, 1.54-5.11) subtypes. CONCLUSIONS: This study provides evidence that a pro-inflammatory diet is associated with an increased risk of GA in Brazil. E-DII requires the inclusion of sodium due to its importance in carcinogenesis.

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The lifetime risk of developing atrial fibrillation (AF) is 1 in 3 adults, resulting in a prevalence of 2-4%. Rheumatic heart disease (RHD) is a frequent aetiology of valvular heart disease in lowand middle-income countries. Between 21% and 80% of patients with mitral valve disease, especially with stenosis, may have AF. Both these conditions, AF and RHD, present a state of persistent inflammation. In turn, inflammation is a frequent cause of anisocytosis, which can be evidenced through the parameter RDW (red bold cell distribution width). Factors associated with increased RDW are also known as risk factors associated with a higher incidence of AF. RDW may have an independent role in the pathogenesis of AF and the increased propensity of both thromboembolic and bleeding events. Another marker involved in the incidence of AF is the neutrophil-lymphocyte ratio. This is also a marker of oxidative stress and inflammation and is associated with a higher rate of AF recurrence. This review will evaluate these biomarkers and their association with cardiovascular events in patients with AF and RHD. The hypotheses and current debates about the relationship of biomarkers with the severity of chronic valve dysfunction, with acute rheumatic carditis in the paediatric population, and with the presence of thrombus in the left atrium will be discussed.

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