Necropolitics of Death in Neurodegeneration.

Neurodegenerative diseases (ND) pose significant challenges for biomedicine in the twenty-first century, particularly considering the global demographic ageing and the subsequent increase in their prevalence. Characterized as progressive, chronic and debilitating, they often result in higher mortality rates compared with the general population. Research agendas and biomedical technologies are shaped by power relations, ultimately affecting patient wellbeing and care. Drawing on the concepts of bio- and necropolitics, introduced by philosophers Foucault and Mbembe, respectively, this perspective examines the interplay between the territoriality and governmentality around demographic ageing, ND and death, focussing on knowledge production as a dispositif of power by highlighting the marginal role that the phenomenon of mortality plays in the ND research landscape. We propose a shift into acknowledging the coloniality of knowledge and embracing its situatedness to attain knowledge 'from death', understood as an epistemic position from which novel approaches and practices could emerge.

A data-driven model for COVID-19 pandemic - Evolution of the attack rate and prognosis for Brazil.

We introduce a compartmental model SEIAHRV (Susceptible, Exposed, Infected, Asymptomatic, Hospitalized, Recovered, Vaccinated) with age structure for the spread of the SARAS-CoV virus. In order to model current different vaccines we use compartments for individuals vaccinated with one and two doses without vaccine failure and a compartment for vaccinated individual with vaccine failure. The model allows to consider any number of different vaccines with different efficacies and delays between doses. Contacts among age groups are modeled by a contact matrix and the contagion matrix is obtained from a probability of contagion p c per contact. The model uses known epidemiological parameters and the time dependent probability p c is obtained by fitting the model output to the series of deaths in each locality, and reflects non-pharmaceutical interventions. As a benchmark the output of the model is compared to two good quality serological surveys, and applied to study the evolution of the COVID-19 pandemic in the main Brazilian cities with a total population of more than one million. We also discuss with some detail the case of the city of Manaus which raised special attention due to a previous report of We also estimate the attack rate, the total proportion of cases (symptomatic and asymptomatic) with respect to the total population, for all Brazilian states since the beginning of the COVID-19 pandemic. We argue that the model present here is relevant to assessing present policies not only in Brazil but also in any place where good serological surveys are not available.

Periodic weakness of the diaphragm as the sole manifestation of bulbar onset myasthenia.

No abstract provided.

Lovastatin decreases the synthesis of inflammatory mediators during epileptogenesis in the hippocampus of rats submitted to pilocarpine-induced epilepsy.

Statins may act on inflammatory responses, decreasing oxidative stress and also reducing brain inflammation in several brain disorders. Epileptogenesis is a process in which a healthy brain becomes abnormal and predisposed to generating spontaneous seizures. We previously reported that lovastatin could prevent neuroinflammation in pilocarpine-induced status epilepticus (SE). In this context, this study investigated the long-lasting effects of lovastatin on mRNA expression of proinflammatory cytokines (interleukin-1ß, tumor necrosis factor α, interleukin-6) and the antiinflammatory cytokine IL-10 in the hippocampus during epileptogenesis by immunohistochemistry and real time polymerase chain reaction (RT-PCR) during the latent and chronic phases in the epilepsy model induced by pilocarpine in rats. For these purposes, four groups of rats were employed: saline (CONTROL), lovastatin (LOVA), pilocarpine (PILO), and pilocarpine plus lovastatin (PILO+LOVA). After pilocarpine injection (350mg/kg, i.p.), the rats were treated with 20mg/kg of lovastatin via an esophagic probe 2h after SE onset. All surviving rats were continuously treated during 15days, twice/day. The pilocarpine plus lovastatin group showed a significant decrease in the levels of IL-1ß, TNF-α, and IL-6 during the latent phase and a decreased expression of IL-1ß and TNF-α in the chronic phase when compared with the PILO group. Moreover, lovastatin treatment also induced an increased expression of the antiinflammatory cytokine, IL-10, in the PILO+LOVA group when compared with the PILO group in the chronic phase. Thus, our data suggest that lovastin may reduce excitotoxicity during epileptogenesis induced by pilocarpine by increasing the synthesis of IL-10 and decreasing proinflammatory cytokines in the hippocampus.

Outcome of SARS-CoV-2 associated Guillain-Barre syndrome depends on early treatment and vaccination. / La evolución del síndrome de Guillain-Barré asociado al SARS-CoV-2 depende del tratamiento temprano y de la vacunación.

TITLE: La evolución del síndrome de Guillain-Barré asociado al SARS-CoV-2 depende del tratamiento temprano y de la vacunación.