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Calderon-Garciduenas L.,University of Montana | Franco-Lira M.,Hospital Central Militar | Mora-Tiscareno A.,Instituto Nacional Of Pediatria | Medina-Cortina H.,Instituto Nacional Of Pediatria | And 2 more authors.
BioMed Research International | Year: 2013

Chronic exposure to particulate matter air pollution is known to cause inflammation leading to respiratory- and cardiovascular-related sickness and death. Mexico City Metropolitan Area children exhibit an early brain imbalance in genes involved in oxidative stress, inflammation, and innate and adaptive immune responses. Early dysregulated neuroinflammation, brain microvascular damage, production of potent vasoconstrictors, and perturbations in the integrity of the neurovascular unit likely contribute to progressive neurodegenerative processes. The accumulation of misfolded proteins coincides with the anatomical distribution observed in the early stages of both Alzheimer's and Parkinson's diseases. We contend misfolding of hyperphosphorylated tau (HPπ), alpha-synuclein, and beta-amyloid could represent a compensatory early protective response to the sustained systemic and brain inflammation. However, we favor the view that the chronic systemic and brain dysregulated inflammation and the diffuse vascular damage contribute to the establishment of neurodegenerative processes with childhood clinical manifestations. Friend turns Foe early; therefore, implementation of neuroprotective measures to ameliorate or stop the inflammatory and neurodegenerative processes is warranted in exposed children. Epidemiological, cognitive, structural, and functional neuroimaging and mechanistic studies into the association between air pollution exposures and the development of neuroinflammation and neurodegeneration in children are of pressing importance for public health. © 2013 Lilian Calderón-Garcidueñas et al.

Bastida-Alquicira J.,SubseccioN de Ultrasonido | Motta-Ramirez G.A.,SubseccioN de Ultrasonido | Amezquita-Perez S.,SubseccioN de Ultrasonido | Gomez-Vazquez J.A.,Hospital Central Militar
Medicina Interna de Mexico | Year: 2015

Contrast media induced nephropathy (CIN) is attributed to several factors: the use of hyperosmolar contrast media, the number of studies with contrast especially if intra-arterial, diseases that decrease renal perfusion per se, as diabetes and hypertension, and the use of nephrotoxic drugs, among others. Current literature was review seeking review studies on the radiological contrasts pathogenesis of adverse reactions, associated event types, risk groups, diagnosis and conduct to follow. Contrast media have been considered the main cause of renal disease in hospitalized patients, not forgetting the outpatient. In most recent research study of contrast media induced nephropathy, this is overdiagnosed and confused of associated nephrotoxic effects that determine events. However, there is evidence that at least in patients with severe renal impairment (glomerular filtration rate <30 mL/min/1.73 m2), contrast media of low or iso-osmolar are potentially nephrotoxic, which should keep watching them and appreciating its relationship with the contrast media induced nephropathy. It is important to recognize the clinical patient factors and the type and manner of application of the contrast medium and its relation to the contrast media induced nephropathy. In all patients, risk factors should be identified so that the dose of contrast is decreased and the necessary preventive measures are taken to prevent contrast media induced nephropathy.

Ordonez-Razo R.M.,Centro Medico Nacional Siglo XXI | Garrido-Garduno M.H.,Centro Medico Nacional Siglo XXI | Ruiz V.M.,Instituto Nacional Of Enfermedades Respiratorias Ismael Cosio Villegas | Herrera-Tepatlan E.,Hospital Central Militar | And 4 more authors.
Genetic Testing and Molecular Biomarkers | Year: 2012

Background: The C allele of c.-94C>G polymorphism of the delta-sarcoglycan gene was associated as a risk factor for coronary spasm in Japanese patients with hypertrophic cardiomyopathy (HCM). Aim: We evaluated whether the c.-94C>G polymorphism can be a risk factor for HCM in Mexican patients. Methods: The polymorphism was genotyped and the risk was estimated in 35 HCM patients and 145 healthy unrelated individuals. Data of this polymorphism reported in Mexican Amerindian populations were included. Results: The C allele frequency in HCM patients was higher with an odds ratio (OR) of 2.37, and the risk for the CC genotype increased to 5.0. The analysis with Mexican Amerindian populations showed that the C allele frequency was significantly higher in HCM patients with an OR of 2.96 and for CC genotype the risk increased to 7.60. Conclusions: The C allele of the c.-94C>G polymorphism is a risk factor for HCM, which is increased by the Amerindian component and can play an important role in the etiology and progression of disease in Mexican patients. © 2012 Mary Ann Liebert, Inc.

Carrasco Vargas H.,Sala de Neurologia | Castellanos Rodriguez J.,Escuela Militar de Graduados de Sanidad | Aceves Rodriguez R.,Hospital Central Militar
Neurologia, Neurocirugia y Psiquiatria | Year: 2011

Introduction. Essential tremor is probably the most frequent movement disorder, particularly among the senile population. It can affect the ability to perform the daily living activities in such a way, that patients frequently need family help for simple tasks such as getting dressed, feeding and so on. Patients frequently get socially isolated. Material and method. Results. Current treatments include propranolol, a beta-channel blocker and primidone, a barbiturate, which can produce improvement in 40% to 50% of the patients. These drugs have many adverse side effects in diabetic or cardiovascular patients. Because of this, new therapies with less side effects are needed. Conclusion. In this study, topiramate demonstrated efficacy in the treatment of essential tremor with the advantage of being safe at any age group, or in patients with diabetes or cardiovascular problems, two very frequent situations in Mexican population.

Calderon-Garciduenas L.,University of Montana | Vojdani A.,Immunosciences Laboratory | Blaurock-Busch E.,MTM Laboratories | Busch Y.,MTM Laboratories | And 7 more authors.
Journal of Alzheimer's Disease | Year: 2015

Millions of children are exposed to concentrations of air pollutants, including fine particulate matter (PM2.5), above safety standards. In the Mexico City Metropolitan Area (MCMA) megacity, children show an early brain imbalance in oxidative stress, inflammation, innate and adaptive immune response-associated genes, and blood-brain barrier breakdown. We investigated serum and cerebrospinal fluid (CSF) antibodies to neural and tight junction proteins and environmental pollutants in 139 children ages 11.91 ± 4.2 y with high versus low air pollution exposures. We also measured metals in serum and CSF. MCMA children showed significantly higher serum actin IgG, occludin/zonulin 1 IgA, IgG, myelin oligodendrocyte glycoprotein IgG and IgM (p < 0.01), myelin basic protein IgA and IgG, S-100 IgG and IgM, and cerebellar IgG (p < 0.001). Serum IgG antibodies to formaldehyde, benzene, and bisphenol A, and concentrations of Ni and Cd were significantly higher in exposed children (p < 0.001). CSF MBP antibodies and nickel concentrations were higher in MCMA children (p = 0.03). Air pollution exposure damages epithelial and endothelial barriers and is a robust trigger of tight junction and neural antibodies. Cryptic 'self' tight junction antigens can trigger an autoimmune response potentially contributing to the neuroinflammatory and Alzheimer and Parkinson's pathology hallmarks present in megacity children. The major factor determining the impact of neural antibodies is the integrity of the blood-brain barrier. Defining the air pollution linkage of the brain/immune system interactions and damage to physical and immunological barriers with short and long term neural detrimental effects to children's brains ought to be of pressing importance for public health. © 2015-IOS Press and the authors.

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