Sex differences in vanadium inhalation effects in non-ciliated bronchiolar cells

The non-ciliated bronchiolar cell (NCBC) is responsible for the defense of the lung and responds to negative stimuli such as exposure to toxic pro-oxidant substances, which triggers the hyperproduction and hypersecretion of mucins and CC16 protein. The literature demonstrates that physiological and pathological responses in the lung can be influenced by the organism’s sex. The objective of this report was to evaluate response differences to vanadium inhalation in male and female CD-1 mice. Mice were exposed to vanadium for four weeks. Hyperplasia of bronchiolar epithelium, small inflammatory foci and sloughing of the NCBC were observed, without changes between sexes and throughout the exposure time. Mucosecretory metaplasia was found in both males and females, however it was more drastic in males. The expression of CC16 increased in both sexes. This study demonstrated a different susceptibility between male and female mice exposed to vanadium inhalation regarding mucosecretory metaplasia

Oxidative Stress and Vanadium

Air pollution is a worldwide health problem, and metals are one of the various air pollutants to which living creatures are exposed. The pollution by metals such as: lead, cadmium, manganese, and vanadium have a common mechanism of action: the production of oxidative stress in the cell. Oxidative stress favors the production of free radicals, which damage biomolecules such as: DNA, proteins, lipids, and carbohydrates; these free radicals produce changes that are observed in different organs and systems. Vanadium is a transition element delivered into the atmosphere by the combustion of fossil fuels as oxides and adhered to the PM enters into the respiratory system, then crosses the alveolar wall and enters into the systemic circulation. In this chapter, we will review the oxidative stress induced by vanadium—as a common mechanism of metal pollutants—; in addition, we will review the protective effect of the antioxidants (carnosine and ascorbate)

Large Cerebellar Stroke in a Young COVID-19-Positive Patient: Case Report.

BackgroundCoronavirus disease 2019 (COVID-19), caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), most frequently presents with respiratory symptoms, such as fever, dyspnea, shortness of breath, cough, or myalgias. There is now a growing body of evidence that demonstrates that severe SARS-CoV-2 infections can develop clinically significant coagulopathy, inflammation, and cardiomyopathy, which have been implicated in COVID-19-associated cerebrovascular accidents (CVAs).Case reportWe report an uncommon presentation of a 32-year-old man who sustained a large vessel cerebellar stroke associated with a severe COVID-19 infection. He presented with a headache, worse than his usual migraine, dizziness, rotary nystagmus, and dysmetria on examination, but had no respiratory symptoms initially. He was not a candidate for thrombolytic therapy or endovascular therapy and was managed with clopidogrel, aspirin, and atorvastatin. During hospital admission he developed COVID-19-related hypoxia and pneumonia, but ultimately he was discharged to home rehabilitation. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: We present this case to increase awareness among emergency physicians of the growing number of reports of neurologic and vascular complications, such as ischemic CVAs, in otherwise healthy individuals who are diagnosed with SARS-CoV-2 infection. A brief review of the current literature will help elucidate possible mechanisms, risk factors, and current treatments for CVA associated with SARS-CoV-2

Bioactive Peptides against Human Apicomplexan Parasites

Apicomplexan parasites are the causal agents of different medically important diseases, such as toxoplasmosis, cryptosporidiosis, and malaria. Toxoplasmosis is considered a neglected parasitosis, even though it can cause severe cerebral complications and death in immunocompromised patients, including children and pregnant women. Drugs against Toxoplasma gondii, the etiological agent of toxoplasmosis, are highly toxic and lack efficacy in eradicating tissue cysts, promoting the establishment of latent infection and acute relapsing disease. Cryptosporidiosis has been recognized as the most frequent waterborne parasitosis in US outbreaks; anti-cryptosporidium drug discovery still faces a major obstacle: drugs that can act on the epicellular parasite. Severe malaria is most commonly caused by the progression of infection with Plasmodium falciparum. In recent years, great progress has been made in the field of antimalarial drugs and vaccines, although the resistance of P. falciparum to artemisinin has recently gained a foothold in Africa. As seen, the search for new drugs against these parasites remains a challenge. Peptide-based drugs seem to be attractive alternative therapeutic agents recently recognized by the pharmaceutical industry, as they can kill different infectious agents and modulate the immune response. A review of the experimental effects of bioactive peptides on these parasites follows, along with comments. In addition, some biological and metabolomic generalities of the parasites are reviewed to elucidate peptide mechanisms of action on Apicomplexan targets

Changes in the Proliferation of the Neural Progenitor Cells of Adult Mice Chronically Infected with <i>Toxoplasma gondii</i>

During Toxoplasma gondii chronic infection, certain internal factors that trigger the proliferation of neural progenitor cells (NPCs), such as brain inflammation, cell death, and changes in cytokine levels, are observed. NPCs give rise to neuronal cell types in the adult brain of some mammals. NPCs are capable of dividing and differentiating into a restricted repertoire of neuronal and glial cell types. In this study, the proliferation of NPCs was evaluated in CD-1 adult male mice chronically infected with the T. gondii ME49 strain. Histological brain sections from the infected mice were evaluated in order to observe T. gondii tissue cysts. Sagittal and coronal sections from the subventricular zone of the lateral ventricles and from the subgranular zone of the hippocampal dentate gyrus, as well as sagittal sections from the rostral migratory stream, were obtained from infected and non-infected mice previously injected with bromodeoxyuridine (BrdU). A flotation immunofluorescence technique was used to identify BrdU+ NPC. The scanning of BrdU+ cells was conducted using a confocal microscope, and the counting was performed with ImageJ® software (version 1.48q). In all the evaluated zones from the infected mice, a significant proliferation of the NPCs was observed when compared with that of the control group. We concluded that chronic infection with T. gondii increased the proliferation of NPCs in the three evaluated zones. Regardless of the role these cells are playing, our results could be useful to better understand the pathogenesis of chronic toxoplasmosis