Obesity-induced neuroinflammation is a chronic aseptic central nervous system inflammation that presents systemic characteristics associated with increased pro-inflammatory cytokines such as interleukin 1 beta (IL-1β) and interleukin 18 (IL-18) and the presence of microglia and reactive astrogliosis as well as the activation of the NLRP3 inflammasome. The obesity pandemic is associated with lifestyle changes, including an excessive intake of obesogenic foods and decreased physical activity. Brain areas such as the lateral hypothalamus (LH), lateral septum (LS), ventral tegmental area (VTA), and nucleus accumbens (NAcc) have been implicated in the homeostatic and hedonic control of feeding in experimental models of diet-induced obesity. In this context, a chronic lipid intake triggers neuroinflammation in several brain regions such as the hypothalamus, hippocampus, and amygdala. This review aims to present the background defining the significant impact of neuroinflammation and how this, when induced by an obesogenic diet, can affect feeding control, triggering metabolic and neurological alterations.

Alzheimer’s disease (AD) is the main cause of dementia worldwide. Emerging non-invasive treatments such as photobiomodulation target the mitochondria to minimize brain damage, improving cognitive functions. In this work, an experimental design was carried out to evaluate the effect of transcranial light therapy (TLTC) on synaptic plasticity (SP) and cognitive functions in an AD animal model. Twenty-three mice were separated into two general groups: an APP/PS1 (ALZ) transgenic group and a wild-type (WT) group. Each group was randomly subdivided into two subgroups: mice with and without TLTC, depending on whether they would undergo treatment with TLTC. Cognitive function, measured through an object recognition task, showed non-significant improvement after TLTC. SP, on the other hand, was evaluated using four electrophysiological parameters from the Schaffer-CA1 collateral hippocampal synapses: excitatory field potentials (fEPSP), paired pulse facilitation (PPF), long-term depression (LTD), and long-term potentiation (LTP). An improvement was observed in subjects treated with TLTC, showing higher levels of LTP than those transgenic mice that were not exposed to the treatment. Therefore, the results obtained in this work showed that TLTC could be an efficient non-invasive treatment for AD-associated SP deficits.

Paclitaxel, a widely used cancer chemotherapeutic agent, has high incidence of neurotoxicity associated with the production of neuropathic pain, for which only duloxetine has shown significant but moderate analgesic effect. Since statins, classically used to reduce hypercholesterolemia, have shown antinociceptive effect in preclinical studies on neuropathic pain, we studied whether the antinociceptive efficacy of duloxetine could be synergistically potentiated by rosuvastatin in a model of paclitaxel-induced neuropathy in mice. The astrocytic and microglial responses in the spinal cord of paclitaxel-treated mice were also assessed by measuring GFAP and CD11b proteins, respectively. Paclitaxel treatment did not impair motor coordination and balance in rotarod testing. Rosuvastatin, duloxetine, and the rosuvastatin/duloxetine combination (combined at equieffective doses) dose-dependently decreased mechanical allodynia (ED₃₀, von Frey testing) and thermal hyperalgesia (ED₅₀, hot plate testing) in paclitaxel-treated mice. Isobolographic analysis showed a superadditive interaction for rosuvastatin and duloxetine, as both the ED₃₀ and ED₅₀ for the rosuvastatin/duloxetine combination contained only a quarter of each drug compared to the individual drugs. The rosuvastatin/duloxetine combination reversed paclitaxel-induced GFAP overexpression, indicating that such effects might depend in part on astrocyte inactivation. Results suggest that statins could be useful in synergistically enhancing the efficacy of duloxetine in some chemotherapy-induced neuropathic conditions.

En este artículo presentamos una experiencia piloto de innovación referida al Prácticum, realizada en la E. de Magisterio de la UAH., durante los cursos 2006-07 y 2007-08. La experiencia, que parte de la premisa de formar un profesor crítico y con criterio, nos ha llevado a situarnos en el modelo del profesor refl exivo. Empezamos indicando el origen de la propuesta, y más tarde justifi camos las bases del modelo, explicamos la metodología que hemos empleado e indicamos las conclusiones que se derivan de la experiencia.

Trypanosoma cruzi, the protozoan causative of Chagas disease, is primarily transmitted through blood-sucking insects and infects mammalian and some reptilian hosts. In Chile, insects of the Mepraia genus are key vectors of T. cruzi in its wild transmission cycle. High prevalence and mixed infection of T. cruzi lineages have been reported in a Mepraia population on Santa María Island in the Atacama Desert. However, no small mammals have been reported. The island’s vertebrate community is dominated by the lizard Microlophus atacamensis and marine and scavenger birds. This study aimed to research blood samples of M. atacamensis for the presence of T. cruzi DNA (kDNA and satDNA) using conventional PCR (cPCR) and quantitative real-time PCR (qPCR) and estimate parasitemia. Our findings reveal that 39.4% of 33 individuals were positive with both cPCR and qPCR, while when assessing infection with either technique, it rises up to 81.8%. These findings confirm that M. atacamensis is a host of T. cruzi, suggesting its potential role as a key reservoir in the island’s transmission cycle. This study provides new insights into the life cycle of T. cruzi in the coastal Atacama Desert, highlighting the importance of reptiles in the epidemiology of this parasite.

Racehorses are subjected to intensive training, often leading to musculoskeletal injuries that require management with non-steroidal anti-inflammatory drugs (NSAIDs). In Chile, the Consejo Nacional de la Hípica regulates equine sports and classifies NSAIDs, including phenylbutazone (PBZ), as doping agents. However, current pharmacokinetic data are limited, relying on small sample sizes that may affect their applicability. This study evaluated the elimination pharmacokinetics of IV-administered PBZ (4.4 mg/kg) in two groups of Thoroughbred racehorses: pre-competition horses (5 years). In the younger group, the elimination half-life was 3.69 h, C₀ was 17.58 mg/L, volume of distribution was 180 L, and clearance was 34.35 L/h, while in the older group, these values were 3.5 h, 19.62 mg/L, 108 L, and 27.95 L/h, respectively, with no significant differences between groups. These findings suggest that PBZ elimination kinetics are comparable across different age groups and provide relevant evidence for the formulation of regulatory policies in the field of equine sports medicine.