Population Characteristics of Human-Commensal Rodents Present in Households from Mérida, Yucatán, México

Anthropocommensal rodents live in close proximity to humans in many habitats around the world. They are a threat to public health because of the pathogens they carry. Recent studies in Mérida, Yucatán, México, have shown that commensal rodents harbor potential zoonotic pathogens such as bacteria, helminths, and viruses. In this study, we describe reproductive and demographic parameters of house mice and black rats present in households from Mérida, Yucatán, México, a municipality located in a tropical region in southern México. Rodents were trapped in 142 households within the municipality of Mérida from 2011 to 2014. A total of 832 rodents were trapped, constituting 556 (66.8%) house mice (Mus musculus) and 276 (33.2%) black rats (Rattus rattus). The sex ratio in mice was different than parity, while in rats it was 1:1. Mice in the weight class 8.1–12 g were most abundant in both females (52.9%) and males (57.2%). On the other hand, rats weighing ≤ 40 g (25% of females and 28.6% of males) were most abundant. The percentage of pregnancy in mice was 46.7%, whereas in rats it was 21.3%. The mean number of embryos was 4.7 and 5.8 in mice and rats, respectively. This study provides relevant demographic information on the ecology of commensal rodents from a tropical region of Latin America. We consider that our findings could be useful as a first step toward understanding the ecological behavior of rodent populations in tropical regions

Heptanoate is neuroprotective in vitro but triheptanoin post-treatment did not protect against middle cerebral artery occlusion in rats

Triheptanoin, the medium-chain triglyceride of heptanoate, has been shown to be anticonvulsant and neuroprotective in several neurological disorders. In the gastrointestinal tract, triheptanoin is cleaved to heptanoate, which is then taken up by the blood and most tissues, including liver, heart and brain. Here we evaluated the neuroprotective effects of heptanoate and its effects on mitochondrial oxygen consumption in vitro. We also investigated the neuroprotective effects of triheptanoin compared to long-chain triglycerides when administered after stroke onset in rats. Heptanoate pre-treatment protected cultured neurons against cell death induced by oxygen glucose deprivation and N-methyl-D-aspartate. Incubation of cultured astrocytes with heptanoate for 2 h increased mitochondrial proton leak and also enhanced basal respiration and ATP turnover, suggesting that heptanoate protects against oxidative stress and is used as fuel. However, continuous 72 h infusion of triheptanoin initiated 1 h after middle cerebral artery occlusion in rats did not alter stroke volume at 3 days or neurological deficit at 1 and 3 days relative to long-chain triglyceride control treatment

Devolution and National Identity Formation in Spain

(Statement of Responsibility) by Silvia Manzanero(Thesis) Thesis (B.A.) -- New College of Florida, 2003(Electronic Access) RESTRICTED TO NCF STUDENTS, STAFF, FACULTY, AND ON-CAMPUS USE(Bibliography) Includes bibliographical references.(Source of Description) This bibliographic record is available under the Creative Commons CC0 public domain dedication. The New College of Florida, as creator of this bibliographic record, has waived all rights to it worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law.(Local) Faculty Sponsor: Hicks, Barbar

Iran gets the bomb - then what?

George Perkovich; Silvia Manzaner

The effects of C5aR1 on leukocyte infiltration following pilocarpine-induced status epilepticus

This study aimed to determine the role C5aR1 plays in mediating immune responses acutely after pilocarpine-induced status epilepticus (SE), specifically those of brain-infiltrating leukocytes. Three days following pilocarpine SE, we determined by flow cytometry the brain immune cell phenotypes and measured key proinflammatory and antiinflammatory cytokine expression by infiltrating leukocytes and microglia in C5aR1-deficient and wild-type mice. Absence of C5aR1 reduced by 47% the numbers of Ly6G(+) neutrophils in the brains of No-SE mice and decreased neutrophil entry after SE to levels found in wild-type brains that did not undergo SE (No-SE). Moreover, C5aR1-deficient mice showed increased interleukin (IL)-4 expression in infiltrating leukocytes, but not in microglia. Increases in IL-4 expression in infiltrating leukocytes coupled with decreased neutrophil invasion in C5aR1-deficient mice after SE is likely to contribute to the reduced neuronal loss previously found in these mice compared to their wild-type littermates. Although other SE models need to be investigated to substantiate our findings, this study provides further evidence that C5aR1 is an inflammatory mediator and may play a role in epileptogenesis

Neuronal oxidative stress in acute ischemic stroke: sources and contribution to cell injury

Oxidative stress has emerged as a key deleterious factor in brain ischemia and reperfusion. Malfunction of the oxidative respiratory chain in mitochondria combines with the activation of cytoplasmic oxidases to generate a burst of reactive oxygen species that cannot be neutralized by the cell’s antioxidant mechanisms. As a result, oxidative stress contributes directly to necrosis and apoptosis through a number of pathways in ischemic tissue. Pharmacological intervention with antioxidants or enhancers of endogenous antioxidant molecules is proving to be difficult due to the speed and scope of the oxidative impact. Additionally, the knowledge that neuronal fate in ischemic stroke is tightly linked to other brain cells like endothelial cells and astrocytes has shifted the focus of study from isolated neurons to the neurovascular unit. For this reason, recent efforts have been directed towards understanding the sources of oxidative stress in ischemic stroke and attempting to block the generation of oxygen radicals

Complex alterations in microglial M1/M2 markers during the development of epilepsy in two mouse models

ObjectiveTo characterize the changes in microglial proinflammatory M1 and antiinflammatory M2 marker expression during epileptogenesis in the chronic pilocarpine and intrahippocampal kainate models