Types of chronic conditions combinations and initial cancer treatment among elderly Medicare beneficiaries with localised prostate cancer.

OBJECTIVE: To examine the association between types of chronic conditions combinations and initial cancer treatment among elderly Medicare beneficiaries with localised prostate cancer. METHODS: A population-based retrospective cohort study was conducted using the Surveillance, Epidemiology and End Results (SEER)-Medicare linked database. The study cohort consisted of elderly men (≥ 66 years) with localised prostate cancer diagnosed between 2002 and 2009 (N = 98,264). The initial cancer treatment received during the 6 months after cancer diagnosis consisted of (i) radical prostatectomy (RP); (ii) radiation therapy (RT); (iii) hormone therapy; and (iv) no treatment. Pre-existing chronic conditions were classified into the following eight groups: (i) only cardiometabolic conditions (CM); (ii) only mental health conditions (MH); (iii) only respiratory conditions (RESP); (iv) CM and MH; (v) CM and RESP; (vi) MH and RESP; (vii) all three conditions, CM, MH and RESP; and (viii) none of the three types of conditions. RESULTS: Only 20% did not receive any cancer treatment; 47.4%, 22.1% and 10.5% received RT, RP, and hormone therapy, respectively. In multinomial logistic regression, elderly men with only RESP were more likely to receive RP as compared with those with all the three types of chronic conditions; those with only CM, only RESP, CM and MH or CM and RESP were more likely to receive RT. No significant associations were observed between the receipt of hormone therapy and types of chronic conditions. CONCLUSIONS: A significant proportion of elderly men with chronic conditions have received aggressive initial cancer treatment. Our study findings suggest a conservative approach for the initial prostate cancer treatment among elderly men with significant chronic conditions and localised prostate cancer.

Association between statins and clinical outcomes among men with prostate cancer: a systematic review and meta-analysis.

BACKGROUND: Mixed evidence exists regarding the effects of statins among men with prostate cancer. We aimed to determine the association between statin use and clinical outcomes in prostate cancer using systematic review and meta-analysis. METHODS: Original articles published until second week of August 2015 were searched in electronic databases (Medline-Ovid, Pubmed, Scopus, The Cochrane Library, Web of Science, ProQuest) for studies on statin use in prostate cancer. The main clinical outcomes for the review were: biochemical recurrence (BCR), metastases, and all-cause and prostate cancer-specific mortality. Meta-analysis was performed to calculate the pooled hazard ratio (pHR) and their 95% confidence interval (95% CI). Heterogeneity between the studies was examined using I(2) statistics. Meta-regression was performed, wherever significant heterogeneity was found in the meta-analyses, to find factors associated with poor outcomes, and sensitivity analyses were conducted to assess the robustness of findings. The analyses were conducted using RevMan v5.3, STATA v14, and R v3.1.1. RESULTS: Out of the 1002 retrieved citations, 34 observational cohort studies met the inclusion criteria. Statin use was associated with a 21% reduction in the risk of BCR among those treated with radiation therapy (pHR: 0.79, 95% CI: 0.65, 0.95, P-value=0.01, 10 studies, I(2)=54%), whereas it was not associated with the BCR among those treated with radical prostatectomy (pHR: 0.94, 95% CI: 0.81, 1.09, P-value=0.43, 15 studies, I(2)=65%). Statin use was associated with a 22% reduction in the risk of metastases (pHR: 0.78, 95% CI: 0.68, 0.87, P-value<0.001, 6 studies, I(2)=0%), and a 24% reduction in risk of both all-cause mortality (pHR: 0.76, 95% CI: 0.63, 0.91, P-value=0.004, 6 studies, I(2)=71%), and prostate cancer-specific mortality (pHR: 0.76, 95% CI: 0.64, 0.89, P-value=0.0007, 5 studies, I(2)=40%). CONCLUSIONS: Our systematic review found that statin significantly reduced the all-cause and prostate cancer-specific mortality and improved the BCR in certain subgroup of men with prostate cancer. In future, randomized controlled trials should be conducted to establish efficacy of statins among men with prostate cancer.

Impact of metformin on clinical outcomes among men with prostate cancer: a systematic review and meta-analysis.

BACKGROUND: Conflicting evidence exists regarding the beneficial effects of metformin in prostate cancer. To determine the association between metformin and clinical outcomes in prostate cancer using systematic review and meta-analysis. METHODS: Original articles published in English until third week of July, 2014 were searched in electronic databases (Medline-Ovid, Scopus, The Cochrane Library, Web of Science, ProQuest) for studies on metformin use in prostate cancer. The clinical outcomes assessed were: development of biochemical recurrence, metastases or castration-resistant metastatic cancer, all-cause and prostate cancer-specific mortality. Meta-analysis was performed to calculate the pooled hazard ratio (pHR) and their 95% confidence interval (95% CI). Heterogeneity between the studies was examined using I2 statistics. Sensitivity analysis was conducted to assess the robustness of findings and publication bias was assessed by the Egger's regression asymmetry test and contour plot. RESULTS: Out of 230 retrieved citations, eight retrospective cohort studies and one nested-case-control study met the inclusion criteria. Metformin use was marginally associated with reduction in the risk of biochemical recurrence (pHR: 0.82, 95% CI: 0.67, 1.01, P-value=0.06, I2=25%, five studies). Metformin use was not significantly associated with metastases (pHR: 0.59, 95% 0.30-1.18, P-value=0.14, I2=74%, three studies), all-cause mortality (pHR: 0.86; 95% CI, 0.67, 1.10, P-value=0.23, I2: 73%, six studies) and prostate cancer-specific mortality (pHR: 0.76, 95% CI: 0.43, 1.33, P-value = 0.33, I2=60%, four studies). Pooled estimates for all outcomes varied in sensitivity analysis by diabetes status and primary treatment of prostate cancer. Systematic review revealed mixed findings on metformin use and the risk of CRPC. CONCLUSIONS: Metformin may reduce the risk of biochemical recurrence in prostate cancer. Given the potential of selection bias in the observational studies, randomized trials should be designed to assess the efficacy of metformin use in prostate cancer.

Effect of sugar beet tubers as a partial replacer to green fodder on production performance and economics of lactating Surti buffaloes in lean period.

AIM: The objective of this study was to evaluate the effects of sugar beet tubers as a replacer to green fodder on production performance and economics of lactating Surti buffaloes. MATERIALS AND METHODS: This trial was conducted at the Livestock Research Station, Navsari Agricultural University, Navsari. Twenty lactating Surti buffaloes in a changeover experimental design were selected to assess the effects of replacing green fodder with sugar beet (Beta vulgaris L.) tubers on production performance, economics of feeding sugar beet and blood biochemical profile. Half (50%) of the hybrid Napier was replaced with sliced sugar beet tubers in the ration of experimental animals. RESULTS: Partial replacement of hybrid Napier with that of sugar beet tubers numerically improved dry matter intake, milk yield, 4% fat corrected milk and milk composition parameters such as fat, solid non-fat, protein and lactose, but not significantly. The blood parameters were in normal range and non-significant except that of glucose and triglycerides, which were increased in the sugar beet group. Replacing sugar beet tubers also proved to be cost-effective with improved net profit around Rs. 6.63/day. CONCLUSION: It can be concluded that 50% hybrid Napier fodder can be replaced with sugar beet tubers without any adverse effect on animal production performance, milk composition blood biochemical profile and economics of feeding.

Health-related quality of life in patients with chronic obstructive pulmonary disease in North India.

BACKGROUND AND OBJECTIVES: Chronic obstructive pulmonary disease (COPD) is a major health problem in India and constitutes an important cause of mortality and morbidity. A cross-sectional study was undertaken to assess health-related quality of life (HRQL) and its determinants in patients with COPD from India. MATERIALS AND METHODS: A total of 126 patients (73.81% male) were enrolled using convenient sampling prospectively in this cross-sectional study. Eligible patients were assessed for socioeconomic status, anthropometric measures, COPD severity, dyspnea and health status using the Hindi version of St George's Respiratory Questionnaire (SGRQ). Linear regression model was used to examine the association between risk factors and HRQL score (a higher score indicating poorer HRQL), adjusting for age and sex. RESULTS: The mean total score for SGRQ in the patients was 52.66 ± 12.89, indicating a marked impairment of HRQL. Impairment was associated with the severity of airway obstruction, but within each Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage, the variation (SD) was wide [stage I: 47.8 ± 12.3 (n = 14); stage II: 49.28 ± 11.69 (n = 47); stage III: 53.47 ± 11.69 (n = 44); stage IV: 61.75 ± 14.14 (n = 21)]. A regression analysis showed that body mass index, forced expiratory volume in 1 s (FEV 1 ), dyspnea grade, and depression were associated with poor HRQL. CONCLUSION: HRQL of COPD patients was significantly impaired across stages. Marked impairment of HRQL was found even in patients with mild disease.

A simplified heat transfer model for predicting temperature change inside food package kept in cold room.

A simple analytical heat flow model for a closed rectangular food package containing fruits or vegetables is proposed for predicting time temperature distribution during transient cooling in a controlled environment cold room. It is based on the assumption of only conductive heat transfer inside a closed food package with effective thermal properties, and convective and radiative heat transfer at the outside of the package. The effective thermal conductivity of the food package is determined by evaluating its effective thermal resistance to heat conduction in the packages. Food packages both as an infinite slab and a finite slab have been investigated. The finite slab solution has been obtained as the product of three infinite slab solutions describe in ASHRAE guide and data book. Time temperature variation has been determined and is presented graphically. The cooling rate and the half cooling time were also obtained. These predicted values, are compared with the experimentally measured values for both the finite and infinite closed packages containing oranges. An excellent agreement between them validated the simple proposed model.

Acquired MET expression confers resistance to EGFR inhibition in a mouse model of glioblastoma multiforme.

Glioblastoma multiforme (GBM) is an aggressive brain tumor for which there is no cure. Overexpression of wild-type epidermal growth factor receptor (EGFR) and loss of the tumor suppressor genes Ink4a/Arf and PTEN are salient features of this deadly cancer. Surprisingly, targeted inhibition of EGFR has been clinically disappointing, demonstrating an innate ability for GBM to develop resistance. Efforts at modeling GBM in mice using wild-type EGFR have proven unsuccessful to date, hampering endeavors at understanding molecular mechanisms of therapeutic resistance. Here, we describe a unique genetically engineered mouse model of EGFR-driven gliomagenesis that uses a somatic conditional overexpression and chronic activation of wild-type EGFR in cooperation with deletions in the Ink4a/Arf and PTEN genes in adult brains. Using this model, we establish that chronic activation of wild-type EGFR with a ligand is necessary for generating tumors with histopathological and molecular characteristics of GBMs. We show that these GBMs are resistant to EGFR kinase inhibition and we define this resistance molecularly. Inhibition of EGFR kinase activity using tyrosine kinase inhibitors in GBM tumor cells generates a cytostatic response characterized by a cell cycle arrest, which is accompanied by a substantial change in global gene expression levels. We demonstrate that an important component of this pattern is the transcriptional activation of the MET receptor tyrosine kinase and that pharmacological inhibition of MET overcomes the resistance to EGFR inhibition in these cells. These findings provide important new insights into mechanisms of resistance to EGFR inhibition and suggest that inhibition of multiple targets will be necessary to provide therapeutic benefit for GBM patients.

Nicotine and estrogen synergistically exacerbate cerebral ischemic injury.

The greater incidence of myocardial infarction, cardiac arrest, and ischemic stroke among women who smoke and use oral contraception (OC) compared to women who do not smoke and who do or do not use OC may be due in part to how nicotine influences endocrine function in women. For example, we recently demonstrated that chronic exposure to nicotine, the addictive agent in tobacco smoke responsible for the elevated risk of cardiac arrest, abolishes the endogenous or exogenous 17ß-estradiol-conferred protection of the hippocampus against global cerebral ischemia (a potential outcome of cardiac arrest) in naive or ovariectomized female rats. In the current study we examined the hypotheses that (1) a synergistic deleterious effect of nicotine plus oral contraceptives exacerbates post-ischemic hippocampal damage in female rats, and (2) nicotine directly inhibits estrogen-mediated intracellular signaling in the hippocampus. To test first hypothesis and to simulate smoking behavior-induced nicotine levels in the human body, we implanted osmotic pumps containing nicotine in the female rats for 16 days. Furthermore, we mimicked the use of oral contraceptives in females by administering oral contraceptives orally to the rat. Rats exposed to either nicotine alone or in combination with oral contraceptives were subjected to an episode of cerebral ischemia and the resultant brain damage was quantified. These results showed for the first time that nicotine with oral contraceptives did indeed exacerbate post-ischemic CA1 damage as compared to nicotine alone in naive female rats. In ex vivo hippocampal slice cultures, we found that nicotine alone or with 17ß-estradiol directly hinders estrogen receptors-mediated phosphorylation of cyclic-AMP element binding protein, a process required for neuronal survival and also exacerbates ischemic damage. Thus, nicotine can affect the outcome of cerebral ischemia by influencing brain endocrine function directly rather than through indirect systemic effects.

Post-ischemic activation of protein kinase C ε protects the hippocampus from cerebral ischemic injury via alterations in cerebral blood flow.

Protein kinase C (PKC) is a family of serine/threonine-isozymes that are involved in many signaling events in normal and disease states. Previous studies from our lab have demonstrated that ɛPKC plays a pivotal role in neuroprotection induced by ischemic preconditioning. However, the role of ɛPKC during and after brain ischemia is not clearly defined. Therefore, in the present study, we tested the hypothesis that activation of ɛPKC during an ischemic event is neuroprotective. Furthermore, other studies have demonstrated that ɛPKC mediates cerebral ischemic tolerance in the rat brain by decreasing vascular tone. Thus, we also tested the effects of ɛPKC activation during ischemia on cerebral blood flow (CBF). We found that ψɛ-Receptors for Activated C Kinase (RACK), a ɛPKC-selective peptide activator, injected intravenously 30min before induction of global cerebral ischemia conferred neuroprotection in the CA1 region of the rat hippocampus. Moreover, measurements of CBF before, during, and after cerebral ischemia revealed a significant reduction in the reperfusion phase of rats pretreated with ψɛRACK as compared to Tat peptide (vehicle). Our results suggest that ɛPKC can protect the rat brain against ischemic damage by regulating CBF. Thus, ɛPKC may be one of the treatment modalities against ischemic injury.

Forebrain ischemia triggers GABAergic system degeneration in substantia nigra at chronic stages in rats.

The long-term consequences of forebrain ischemia include delayed Parkinson's syndrome. This study revealed delayed neurodegeneration in the substantia nigra 8 weeks after 12.5 minutes of global ischemia in rat brain. Following neuronal loss of 30-40% in central and dorsolateral striatum at day 3, neuronal damage in the substantia nigra (SN) was assessed at 4-8 weeks using immunohistochemistry for glutamate decarboxylase 67 (GAD67), vesicular GABA transporter (VGAT), and calretinin (CR). At day 56, the optical density of GAD67-, but not VGAT-, immunoreactivity in substantia nigra pars reticulata (SNR)-significantly decreased. CR-neurons concentrated in substantia nigra pars compacta (SNC) were reduced by 27% from day 3 (n = 5) to day 56 (n = 7, ANOVA, p < .01). Movement coordination was impaired at day 56, as evaluated using beam-walking test (time-to-traverse 5.6 ± 1.2 sec versus 11.8 ± 5.4 sec; sham versus ischemia, p < .05, n = 5, and 7, resp.). Our results demonstrate delayed impairment of the GABAergic system components in SN and associated with movement deficits after global ischemia.

Derangements of post-ischemic cerebral blood flow by protein kinase C delta.

Cerebral ischemia causes blood flow derangements characterized by hyperemia (increased cerebral blood flow, CBF) and subsequent hypoperfusion (decreased CBF). We previously demonstrated that protein kinase C delta (δPKC) plays an important role in hippocampal neuronal death after ischemia. However, whether part of this protection is due to the role of δPKC on CBF following cerebral ischemia remains poorly understood. We hypothesized that δPKC exacerbates hyperemia and subsequent hypoperfusion resulting in CBF derangements following ischemia. Sprague-Dawley (SD) rats pretreated with a δPKC specific inhibitor (δV1-1, 0.5 mg/kg) exhibited attenuation of hyperemia and latent hypoperfusion characterized by vasoconstriction followed by vasodilation of microvessels after 2-vessel occlusion plus hypotension measured by 2-photon microscopy. In an asphyxial cardiac arrest model (ACA), SD rats treated with δV1-1 (pre- and post-ischemia) exhibited improved perfusion after 24 h and less hippocampal CA1 neuronal death 7 days after ACA. These results suggest possible therapeutic potential of δPKC in modulating CBF and neuronal damage after cerebral ischemia.

Resveratrol pretreatment protects rat brain from cerebral ischemic damage via a sirtuin 1-uncoupling protein 2 pathway.

Resveratrol is a natural polyphenol found in grapes and wine and has been associated with protective effects against cardiovascular diseases. In vitro, both resveratrol preconditioning (RPC) and ischemic preconditioning (IPC) require activation of sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, to induce neuroprotection against cerebral ischemia. In the present study, we tested two hypotheses: (a) that neuroprotection against cerebral ischemia can be induced by RPC in vivo; and (b) that RPC neuroprotection involves alterations in mitochondrial function via the SIRT1 target mitochondrial uncoupling protein 2 (UCP2). IPC was induced by 2 min of global ischemia (temporary bilateral carotid artery occlusion with hypotension), and RPC, by i.p. injection of resveratrol at 10, 50 and 100 mg/kg dosages. Forty-eight hours later, we compared the neuroprotective efficacy of RPC and IPC in vulnerable cornu ammonis 1 hippocampal pyramidal neurons using a rat model of asphyxial cardiac arrest (ACA). SIRT1 activity was measured using a SIRT1-specific fluorescent enzyme activity assay. In hippocampal mitochondria isolated 48 h after IPC or RPC, we measured UCP2 levels, membrane potential, respiration, and the mitochondrial ATP synthesis efficiency (ADP/O ratio). Both IPC and RPC induced tolerance against brain injury induced by cardiac arrest in this in vivo model. IPC increased SIRT1 activity at 48 h, while RPC increased SIRT1 activity at 1 h but not 48 h after treatment in hippocampus. Resveratrol significantly decreased UCP2 levels by 35% compared to sham-treated rats. The SIRT1-specific inhibitor sirtinol abolished the neuroprotection afforded by RPC and the decrease in UCP2 levels. Finally, RPC significantly increased the ADP/O ratio in hippocampal mitochondria reflecting enhanced ATP synthesis efficiency. In conclusion, in vivo resveratrol pretreatment confers neuroprotection similar to IPC via the SIRT1-UCP2 pathway.

Pretreatment with a single estradiol-17beta bolus activates cyclic-AMP response element binding protein and protects CA1 neurons against global cerebral ischemia.

Estradiol-17beta is released from the ovaries in a cyclic manner during the normal estrous cycle in rats. During the transition from the diestrous to proestrous stage, the 17beta-estradiol increases in blood circulation. We hypothesized that a higher serum level of endogenous 17beta-estradiol would protect hippocampal pyramidal neurons against global cerebral ischemia via activation of the cyclic-AMP response element binding protein (CREB)-mediated signaling cascade. Furthermore, we asked if a single 17beta-estradiol bolus provides protection against ischemia in the absence of endogenous estradiol. To test these hypotheses, rats were subjected to global cerebral ischemia at different stages of the estrous cycle. Ischemia was produced by bilateral carotid occlusion and systemic hypotension. Brains were examined for histopathology at 7 days of reperfusion. Higher serum levels of 17beta-estradiol (at proestrus and estrus stages) correlated with increased immunoreactivity of pCREB in hippocampus and ischemic tolerance. At diestrus, when circulating gonadal hormone concentrations were lowest, the pCREB protein content of hippocampus was reduced and showed the least number of normal neurons after ischemia compared to other stages of the estrous cycle. A similar phosphorylation pattern was also observed for mitogen-activated protein kinase (MAPK) and calcium-calmodulin-dependent protein kinase (CaMKII) in hippocampus. The cyclic variation in ovarian hormones did not reflect phosphorylation of protein kinase B (Akt). To test the efficacy of a single bolus of 17beta-estradiol before ischemia, ovariectomized rats were treated with 17beta-estradiol (5/10/50 microg/kg) or vehicle (oil) and 48/72/96 h later rats were exposed to cerebral ischemia. A single 17beta-estradiol bolus treatment in ovariectomized rats significantly increased CREB mRNA activation and protected CA1 pyramidal neurons against ischemia. These results suggest that an exogenous bolus of 17beta-estradiol to ovariectomized rats protects hippocampus against ischemia via activation of the CREB pathway in a manner similar to the endogenous estrous cycle.

Ischemic preconditioning via epsilon protein kinase C activation requires cyclooxygenase-2 activation in vitro.

The signaling pathway of cyclooxygenase-2 (COX-2) induction following ischemic preconditioning (IPC) in brain remains undefined. To determine role of COX-2 in ischemic preconditioning, we used two in vitro models: mixed cortical neuron/astrocyte cell cultures and organotypic hippocampal slice cultures. We simulated IPC by exposing cell or slice cultures to 1 h or 15 min of oxygen/glucose deprivation (OGD), respectively, 48 h prior to ischemia. To mimic ischemia in vitro, we exposed cell or slice cultures to OGD of 4 h or 40 min, respectively. In cell cultures, these experiments revealed that COX-2 induction peaked at 24 h following IPC in cell culture. Inhibition of COX-2 activation with 50 microM NS-398 (a COX-2 selective inhibitor) abolished IPC-mediated neuroprotection in both in vitro models. Next, we tested whether epsilon protein kinase C (epsilonPKC) and extracellular signal regulated kinase 1/2 (ERK1/2) activation was involved in IPC-mediated neuroprotection and COX-2 expression in cell culture. Cell cultures were treated with an epsilonPKC-specific activating peptide (psiepsilonRACK, 100 nM) for 1 h, and 48 h later were exposed to OGD. epsilonPKC activation increased ERK1/2 phosphorylation and COX-2 induction and conferred neuroprotection similar to IPC. Additionally, inhibition of either epsilonPKC or ERK1/2 activation abolished COX-2 expression and neuroprotection due to ischemic preconditioning. These results demonstrate a crucial role for the epsilonPKC-->ERK1/2-->COX-2 pathway in the induction of neuroprotection via ischemic preconditioning.

Estrogen preconditioning protects the hippocampal CA1 against ischemia.

Estrogen is neuroprotective against ischemia in both in vivo and in vitro injury models. Because of the promising preclinical data on neuroprotection, the Women's Estrogen for Stroke Trial was initiated. The outcomes from this trial were, however, unsuccessful and questions emerged about the safety of chronic estrogen treatment in women. In contrast to the chronic estrogen treatment strategy, the present study aims to investigate: (1) the neuroprotective efficacy of single estrogen pretreatment/preconditioning; and (2) the existence of a similarity between estrogen- and ischemic preconditioning-induced neuroprotection against cerebral ischemia. The efficacy of estrogen was tested in an in vitro model of cerebral ischemia using hippocampal organotypic slice culture system. The hippocampal organotypic slice cultures were generated from female neonatal (9-11 days old) Sprague-Dawley rats. The slices were exposed to estradiol-17beta (0.5, 1, 5 nM) for various durations (1, 2 or 4 h) 48 h prior to ischemia (40 min of oxygen-glucose deprivation). For ischemic preconditioning, slices were exposed to sublethal oxygen-glucose deprivation (15 min), 48 h prior to lethal oxygen-glucose deprivation. Quantification of cell death in hippocampal CA1 region was conducted by using propidium iodide fluorescence staining technique. Results demonstrated that estrogen preconditioning significantly protects the hippocampal CA1 region against ischemia (P<0.001) and mimicked ischemic preconditioning-induced neuroprotection. The propidium iodide fluorescence values of estrogen preconditioning, ischemic preconditioning and ischemia groups were 21+/-2 (mean+/-S.E.M.) (1 nM; 2 h; n=15), 18+/-2 (5 nM; 4 h; n=12), 32+/-3 (n=8), 65+/-3 (n=27), respectively. Further, estrogen preconditioning initiated a calcium-mediated signaling pathway leading to protection of CA1 neurons against ischemia. Future investigations in estrogen preconditioning may suggest new estrogen regimens that avoid potential side effects of chronic estrogen treatment for stroke patients.

Real-time magnetic resonance imaging to guide pediatric endovascular procedures.

Although x-ray fluoroscopy (XRF) has guided diagnostic and therapeutic transcatheter procedures for decades, certain limitations still exist. XRF still visualizes tissue poorly and relies on projection of shadows that do not convey depth information. Adjunctive echocardiography overcomes some of these limitations but still suffers suboptimal or unreliable imaging windows. Furthermore, ionizing radiation exposure in children imparts a cancer risk. An interventional platform using real-time magnetic resonance imaging (MRI) may offer superior image guidance without radiation. Although there are many remaining challenges, but real-time MRI has the potential to revolutionize transcatheter therapeutics.