99 research outputs found
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Taenia Taeniaeformis differential staining on onchospheres with vital dyes under critical temperatures
Ingestion of T.saginata eggs by cattle causes a condition called bovine cysticercosis (BC). Hence, control treatments that inactivate T. saginata eggs would be valuable, which requires accurate in vitro methods for assessment of egg viability. Taenia taeniaeformis, a rodent cestode was used as a model and the affect of 0.5% NaOCl on onchosphere recovery from both untreated and heat treated eggs was investigated. Further, the use of non-vital and vital dyes to assess the egg/onchosphere viability under different heat treatments was also studied. Onchosphere recovery of T. taeniaeformis eggs by exshelling with 0.5% NaOCl for 5, 10 or 20 minutes was assessed that showed quadratic loss in recovered eggs and onchospheres with increased incubation time (p<0.05). Also, the effect of heat on the onchosphere recovery was tested by exposing eggs to 55, 65 or 75° C for 10 minutes. Heat treatment at 75° C resulted in remarkable onchosphere loss when exshelled by 0.5% NaOCl (p<0.05). Non-vital dye acridine orange (AO) or vital dye propidium iodide (PI) stained eggs either peripherally or internally, while vital dye trypan blue (TB) showed only peripheral staining in eggs, but showed variable staining in NaOCl exshelled onchospheres. Preliminary studies at low temperatures indicated differences in the staining behavior of the vital dyes, but not between AO and PI. Experiments at higher temperature (55-95° C) were performed for better resolution of the staining behavior. AO or PI was used directly with heat treated eggs, while TB was used with onchospheres that were exshelled prior to heat treatment. This is because of the onchosphere loss mentioned earlier. Non-linear regression analysis on the obtained percentage internal staining data with each dye by fitting four-parametric sigmoid model showed that T50 for AO was lower that that of PI, which in turn was lower than that of TB. From these findings, the use of vital dyes appears to be an unacceptable means to assess viability of onchospheres within eggs or onchospheral membranes
MicroRNA-301a mediated regulation of Kv4.2 in diabetes: identification of key modulators.
Diabetes is a metabolic disorder that ultimately results in major pathophysiological complications in the cardiovascular system. Diabetics are predisposed to higher incidences of sudden cardiac deaths (SCD). Several studies have associated diabetes as a major underlying risk for heart diseases and its complications. The diabetic heart undergoes remodeling to cope up with the underlying changes, however ultimately fails. In the present study we investigated the changes associated with a key ion channel and transcriptional factors in a diabetic heart model. In the mouse db/db model, we identified key transcriptional regulators and mediators that play important roles in the regulation of ion channel expression. Voltage-gated potassium channel (Kv4.2) is modulated in diabetes and is down regulated. We hypothesized that Kv4.2 expression is altered by potassium channel interacting protein-2 (KChIP2) which is regulated upstream by NFkB and miR-301a. We utilized qRT-PCR analysis and identified the genes that are affected in diabetes in a regional specific manner in the heart. At protein level we identified and validated differential expression of Kv4.2 and KChIP2 along with NFkB in both ventricles of diabetic hearts. In addition, we identified up-regulation of miR-301a in diabetic ventricles. We utilized loss and gain of function approaches to identify and validate the role of miR-301a in regulating Kv4.2. Based on in vivo and in vitro studies we conclude that miR-301a may be a central regulator for the expression of Kv4.2 in diabetes. This miR-301 mediated regulation of Kv4.2 is independent of NFkB and Irx5 and modulates Kv4.2 by direct binding on Kv4.2 3'untranslated region (3'-UTR). Therefore targeting miR-301a may offer new potential for developing therapeutic approaches
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Maternal Bisphenol A Exposure Impacts the Fetal Heart Transcriptome
Conditions during fetal development influence health and disease in adulthood, especially during critical windows of organogenesis. Fetal exposure to the endocrine disrupting chemical, bisphenol A (BPA) affects the development of multiple organ systems in rodents and monkeys. However, effects of BPA exposure on cardiac development have not been assessed. With evidence that maternal BPA is transplacentally delivered to the developing fetus, it becomes imperative to examine the physiological consequences of gestational exposure during primate development. Herein, we evaluate the effects of daily, oral BPA exposure of pregnant rhesus monkeys (Macaca mulatta) on the fetal heart transcriptome. Pregnant monkeys were given daily oral doses (400 µg/kg body weight) of BPA during early (50-100 ± 2 days post conception, dpc) or late (100 ± 2 dpc--term), gestation. At the end of treatment, fetal heart tissues were collected and chamber specific transcriptome expression was assessed using genome-wide microarray. Quantitative real-time PCR was conducted on select genes and ventricular tissue glycogen content was quantified. Our results show that BPA exposure alters transcription of genes that are recognized for their role in cardiac pathophysiologies. Importantly, myosin heavy chain, cardiac isoform alpha (Myh6) was down-regulated in the left ventricle, and 'A Disintegrin and Metalloprotease 12', long isoform (Adam12-l) was up-regulated in both ventricles, and the right atrium of the heart in BPA exposed fetuses. BPA induced alteration of these genes supports the hypothesis that exposure to BPA during fetal development may impact cardiovascular fitness. Our results intensify concerns about the role of BPA in the genesis of human metabolic and cardiovascular diseases
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Positive allosteric modulation of the α7 nicotinic acetylcholine receptor as a treatment for cognitive deficits after traumatic brain injury
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