The desire to “debunk” false information is a shared goal among government, social media platforms, and society. How can organizations determine whether a debunking technique is effective? Noting that simply debunking misinformation may not affect its spread, the user actions (clicking or not clicking on like, share, or comment) on postings need to be studied independently from whether a user finds a posting credible. New debunking techniques are routinely adopted social media platforms. Although popup warnings have been available for quite some time, these warnings have been newly repurposed by some platforms as a debunking tool. As such, this study focused on the effects of message popup warnings on credibility and effectiveness (user actions or inactions).

PurposeDisinformation on social media is a serious issue. This study examines the effects of disinformation on COVID-19 vaccination decision-making to understand how social media users make healthcare decisions when disinformation is presented in their social media feeds. It examines trust in post owners as a moderator on the relationship between information types (i.e. disinformation and factual information) and vaccination decision-making.Design/methodology/approachThis study conducts a scenario-based web survey experiment to collect extensive survey data from social media users.FindingsThis study reveals that information types differently affect social media users' COVID-19 vaccination decision-making and finds a moderating effect of trust in post owners on the relationship between information types and vaccination decision-making. For those who have a high degree of trust in post owners, the effect of information types on vaccination decision-making becomes large. In contrast, information types do not affect the decision-making of those who have a very low degree of trust in post owners. Besides, identification and compliance are found to affect trust in post owners.Originality/valueThis study contributes to the literature on online disinformation and individual healthcare decision-making by demonstrating the effect of disinformation on vaccination decision-making and providing empirical evidence on how trust in post owners impacts the effects of information types on vaccination decision-making. This study focuses on trust in post owners, unlike prior studies that focus on trust in information or social media platforms.

AbstractObjectiveDelayed cardiac tamponade, a life‐threatening complication of pericardial effusion in humans, has rarely been described in large animal models. We report here a pig with cardiac tamponade that developed 29 days after cardiac surgery.Study DesignCase report.AnimalsOne 45‐kg domestic pig.MethodsOpen‐chest surgery was performed on a pig to induce chronic heart failure. At 15 days after surgery, the pig's breathing appeared laboured; induced heart failure was considered the cause. Routine heart failure medications were administered.ResultsOn day 28, the pig's status deteriorated. On day 29, echocardiography performed just before the pig's death showed a large pericardial effusion, mainly in the lateral and anterior walls of the right heart, with several fibre exudation bands. The right heart was severely compressed with an extremely small right ventricle. An emergency sternotomy was unsuccessful. Pathologic examination showed a severely thickened, fibrous pericardium. The pericardial sac was distended (up to 4.5 cm) and was full of dark brown, soft, friable material. Epicardial haemorrhage with a fresh, organised thrombus was noted in the pericardium.ConclusionDelayed tamponade occurring at least 15 days after open‐chest surgery is easy to misdiagnose or overlook in large animal models where attention is often focused on primary pathological model changes. To decrease mortality in animal models, researchers should be aware of potential complications and use the same level of follow‐up monitoring of large animals as in clinical care.

Background Cardiac Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) activation plays a critical role in cardiomyocyte (CM) apoptosis and arrhythmia. Functional ATP-sensitive potassium (K ATP ) channels are essential for cardiac protection during ischemia. In cultured CMs, L5 low-density lipoprotein (LDL) induces apoptosis and QTc prolongation. L5 is a highly electronegative and atherogenic aberrant form of LDL, and its levels are significantly higher in patients with cardiovascular-related diseases. Here, the role of L5 in cardiac injury was studied by evaluating the effects of L5 on CaMKII activity and K ATP channel physiology in CMs. Methods Cultured neonatal rat CMs (NRCMs) were treated with a moderate concentration (ie, 7.5 μg/mL) of L5 or L1 (the least electronegative LDL subfraction). NRCMs were examined for apoptosis and viability, CaMKII activity, and the expression of phosphorylated CaMKIIδ and NOX2/gp91 phox . The function of K ATP and action potentials (APs) was analyzed by using the patch-clamp technique. Results In NRCMs, L5 but not L1 significantly induced cell apoptosis and reduced cell viability. Furthermore, L5 decreased Kir6.2 expression by more than 50%. Patch-clamp analysis showed that L5 reduced the K ATP current (I KATP ) density induced by pinacidil, a K ATP opener. The partial recovery of the inward potassium current during pinacidil washout was susceptible to subsequent inhibition by the I KATP blocker glibenclamide. Suppression of I KATP by L5 significantly prolonged the AP duration. L5 also significantly increased the activity of CaMKII, the phosphorylation of CaMKIIδ, and the expression of NOX2/gp91 phox . L5-induced apoptosis was prevented by the addition of the CaMKII inhibitor KN93 and the reactive oxygen species scavenger Mn (III)TBAP. Conclusions L5 but not L1 induces CM damage through the activation of the CaMKII pathway and increases arrhythmogenicity in CMs by modulating the AP duration. These results help to explain the harmful effects of L5 in cardiovascular-related disease.

Background: Myocardial scarring after infarction (MI) can create areas of slowed conduction, which can lead to re-excitation of the heart, or re-entry. Reentrant arrhythmia is one of the electrophysiological mechanisms responsible for ventricular tachycardia after acute myocardial infarction (AMI). Since the sodium channel (Na v 1.5) is a major contributor to cardiac electrical conduction, the objective of this study was to evaluate the effect of cell substrate stiffness on the kinetics of the Na v 1.5. Methods: MI was created by permanent ligation of the left anterior descending artery in rats. After 7 days, hearts were decellularized and grossed into 1 mm rings for measuring stiffness by using an atomic force microscope. The hearts had an elastic modulus of 263.33±76.8 kPa at scar, and 27.26±3.97 kPa at a remote area (n=3). The surface of p olydimethylsiloxane (PDMS) gels was tuned to match the stiffness of decellularized infarcted rat hearts (17.04±2.02 kPa, 110.56±8.70 kPa and 328.4±45.72 kPa, respectively, n=3). Human embryonic kidney 293 (HEK-293) cells were induced to stably express human Na v 1.5. HEK-293 and human pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) were separately cultured on the PDMS substrate that mimicked stiffness of infarcted rat hearts for 24 h. Sodium channel currents (I Na ) and action potentials (APs) were recorded by patch clamp techniques. Results: As substrate stiffness increased, HEK-293 voltage dependent activation of Na v 1.5 (I Na ) shifted significantly towards more positive voltage (Vhalf: -28.42±5.12 mV, -33.47±6.98 mV, -19.84±5.24 mV, respectively, p<0.01 in one-way ANOVA, n=12), and the transition from closed-state into inactivation was faster (tau: 48.47±4.60ms, 40.67±8.07ms, 81.20±9.54ms, p<0.05, n=12). However, the current density, the steady-state inactivation curve and the recovery time were comparable between different PDMS. In iPSC-CMs, the slope of AP upstroke was decreased when stiffness was increased (30.00±1.38V/s, 23.91±0.65V/s, 20.93±0.34V/s, p<0.05, n=15). Conclusion: Increased substrate stiffness, similar to myocardial scar, alters the kinetics of Na v 1.5 and affects the depolarization of cardiomyocytes, which likely contributes to slow conduction after MI.

BACKGROUNDThe association between the early repolarization pattern (ERP) and ventricular arrhythmias in patients with ST-segment elevation myocardial infarction (STEMI) remains uncertain. We hypothesized that ERP predicts the risk of sustained ventricular tachycardia (VT)/ventricular fibrillation (VF) during the acute phase of anterior STEMI.Methods and Results:We enrolled 1,460 consecutive patients with acute anterior STEMI. We identified an ERP-positive group and a 1:6 propensity-matched ERP-negative group of 183 and 471, respectively. Comparisons of sustained VT/VF, heart failure, major adverse cardiovascular events and all-cause death were based on Kaplan-Meier survival analysis and multivariable Cox proportional hazards regression with adjustment for unmatched confounding factors. In our full matching propensity score cohorts, there were 8 out of 28 variables not matching between the 2 groups. The Kaplan-Meier curves showed ERP increased the risk of sustained VT/VF in 30 days (log-rank test P=0.00065). Adjusted for baseline unmatched confounding risk, the Cox hazards regression analysis showed sustained VT/VF was associated with the present of ERP (hazard ratio=2.915, 95% CI: 1.520-5.588, P=0.001).CONCLUSIONSIn a propensity score-adjusted cohort the presence of ERP had a multivariable-adjusted association with increased risk of sustained VT/VF in patients with anterior STEMI in the early 30 days.

The stiffness of myocardial tissue changes significantly at birth and during neonatal development, concurrent with significant changes in contractile and electrical maturation of cardiomyocytes. Previous studies by our group have shown that cardiomyocytes generate maximum contractile force when cultured on a substrate with a stiffness approximating native cardiac tissue. However, effects of substrate stiffness on the electrophysiology and ion currents in cardiomyocytes have not been fully characterized. In this study, neonatal rat ventricular myocytes were cultured on the surface of flat polyacrylamide hydrogels with elastic moduli ranging from 1 to 25 kPa. Using whole-cell patch clamping, action potentials and L-type calcium currents were recorded. Cardiomyocytes cultured on hydrogels with a 9 kPa elastic modulus, similar to that of native myocardium, had the longest action potential duration. Additionally, the voltage at maximum calcium flux significantly decreased in cardiomyocytes on hydrogels with an elastic modulus higher than 9 kPa, and the mean inactivation voltage decreased with increasing stiffness. Interestingly, the expression of the L-type calcium channel subunit α gene and channel localization did not change with stiffness. Substrate stiffness significantly affects action potential length and calcium flux in cultured neonatal rat cardiomyocytes in a manner that may be unrelated to calcium channel expression. These results may explain functional differences in cardiomyocytes resulting from changes in the elastic modulus of the extracellular matrix, as observed during embryonic development, in ischemic regions of the heart after myocardial infarction, and during dilated cardiomyopathy.

Background Vagal hyperactivity promotes atrial fibrillation (AF), which has been almost exclusively attributed to acetylcholine. Vasoactive intestinal polypeptide (VIP) and acetylcholine are neurotransmitters co-released during vagal stimulation. Exogenous VIP has been shown to promote AF by shortening action potential duration (APD), increasing APD spatial heterogeneity, and causing intra-atrial conduction block. Objective The purpose of this study was to investigate the effects of neuronally released VIP on atrial electrophysiologic properties during vagal stimulation. Methods We used a specific VIP antagonist (H9935) to uncover the effects of endogenous VIP released during vagal stimulation in canine hearts. Results H9935 significantly attenuated (1) the vagally induced shortening of atrial effective refractory period and widening of atrial vulnerability window during stimulation of cervical vagosympathetic trunks (VCNS) and (2) vagal effects on APD during stimulation through fat-pad ganglion plexus (VGPS). Atropine completely abolished these vagal effects during VCNS and VGPS. In contrast, VGPS-induced slowing of local conduction velocity was completely abolished by either VIP antagonist or atropine. In pacing-induced AF during VGPS, maximal dominant frequencies and their spatial gradients were reduced significantly by H9935 and, more pronouncedly, by atropine. Furthermore, VIP release in the atria during vagal stimulation was inhibited by atropine, which may account for the concealment of VIP effects with muscarinic blockade. Conclusion Neuronally released VIP contributes to vagal effects on atrial electrophysiologic properties and affects the pathophysiology of vagally induced AF. Neuronal release of VIP in the atria is inhibited by muscarinic blockade, a novel mechanism by which VIP effects are concealed by atropine during vagal stimulation.

Management of data with a time dimension increases the overhead of storage and query processing in large database applications especially with the join operation, which is a commonly used and expensive relational operator. The join evaluation can be time consuming because temporal data are intrinsically multidimensional. The problem can be even harder since tuples with longer life spans tend to overlap a greater number of joining tuples thus; they are likely to be accessed more often. The proposed Adaptive Replacement Cache-Temporal Data (ARC-TD) buffer replacement policy is built upon the Adaptive Replacement Cache (ARC) policy by favoring the cache retention of data pages in proportion to the average life span of the tuples in the buffer. By giving preference to tuples having long life spans, a higher cache hit ratio can be achieved. The caching priority is also balanced between recently and frequently accessed data. An evaluation and comparison study of the proposed ARC-TD algorithm determined the relative performance with respect to a nested-loop join, a sort-merge, and a partition-based join algorithm. The metrics include the processing time (disk I/O time plus CPU time), cache hit ratio, and index storage size. The study was conducted with comparisons in terms of the Least Recently Used (LRU), Least Frequently Used (LFU), ARC, and the new ARC-TD buffer replacement policy.

Management of data with a time dimension increases the overhead of storage and query processing in large database applications especially with the join operation, which is a commonly used and expensive relational operator. The temporal join evaluation can be time consuming because temporal data are intrinsically multi-dimensional. Also, due to a limited buffer size, the long-lived data can be frequently swapped-in and swapped-out between disk and main memory thus resulting in a low cache hit ratio. The proposed index-based Hilbert-Temporal Join (Hilbert-TJ) join algorithm maps temporal data into Hilbert curve space that is inherently clustered, thus allowing for fast retrieval and storage. This paper also proposes the Adaptive Replacement Cache-Temporal Data (ARC-TD) buffer replacement policy which favors the cache retention of data pages in proportion to the average life span of the tuples in the buffer. By giving preference to tuples having long life spans, a higher cache hit ratio can be achieved. The caching priority is also balanced between recently and frequently accessed data. The comparison study consists of different join algorithms and buffer replacement policies. Additionally, the Hilbert-TJ algorithm offers support to both valid-time and transaction-time data.

Management of data with a time dimension increases the overhead of storage and query processing in large database applications especially with the join operation, which is a commonly used and expensive relational operator. The join evaluation is difficult because temporal data are intrinsically multidimensional. The problem is harder since tuples with longer life spans tend to overlap a greater number of joining tuples thus; they are likely to be accessed more often. The proposed index-based Hilbert-Temporal Join (Hilbert-TJ) join algorithm maps temporal data into Hilbert curve space that is inherently clustered, thus allowing for fast retrieval and storage. An evaluation and comparison study of the proposed Hilbert-TJ algorithm determined the relative performance with respect to a nested-loop join, a sort-merge, and a partition-based join algorithm that use a multiversion B+ tree (MVBT) index. The metrics include the processing time (disk I/O time plus CPU time) and index storage size. Under the given conditions, the expected outcome was that by reducing index redundancy better performance was achieved. Additionally, the Hilbert-TJ algorithm offers support to both valid-time and transaction-time data.

The most plausible explanation for the link between CD and cardiomyopathy is that both conditions might be mediated through inflammation and autoimmune mechanisms [5]. Nutritional deficiencies might be a further explanation for the association between cardiomyopathy and CD. Folate deficiency, like in our patient, was found in 20% of adults with newly diagnosed CD [9]. In animal experiments, folate deficiency has been shown to cause myocardial thickening and cardiomyopathy [10]. If folate deficiency plays a role in the development of LVHT is unknown. From our findings we conclude that LVHT may be associated with CD, folate deficiency and stroke. If this association is a pure coincidence or due to a common etiologic factor remains unknown. Since CD is frequently overlooked and is treatable by gluten-free diet, efforts should be made to discover this disease in patients with cardiomyopathies including LVHT. Patients with LVHT and chronic gastrointestinal symptoms should be investigated for CD. The role of folate deficiency in the etiology of cardiomyopathies including LVHT needs to be investigated. The authors report no relationships that could be construed as a conflict of interest. References

Background: There has been increasing evidence that complex interactions among the various components of intracardiac neural network play an important role in atrial fibrillation (AF). Perfusion of vasoactive intestine polypeptide (VIP), a neural polypeptide, co-released with acetylcholine from intrinsic cardiac neurons during vagal stimulation, was shown to shorten the action potential duration (APD), decrease the intraatrial conduction velocity (CV), and promote induction of AF. However, the effect of endogenous VIP remains unclear. Methods: In 6 isolated arterially perfused canine left atria, high-resolution optical mapping techniques with di-4-ANEPPS and blebbistatin were used to measure APD and CV during fat-pad ganglion plexus stimulation (GPS, 30Hz, 10.2±2.3Volt validated with blockage of atrioventricular conduction), at during H9935, a VIP antagonist (1 μM) perfusion. The atria were paced at 200beats per minute. Metoprolol (1.8μM) was used to block the sympathetic effects. Results: Average APD was shorter (21%) during GPS compared to the baseline (100±8ms vs. 126±7ms, p<0.05), and average CV was slower than baseline (87±10cm/sec vs. 103±13cm/sec, p<0.05), which recovered within 2 min (APD: 128±8ms, p<0.05; CV: 105±13cm/sec, p<0.05). With H9335, the APD shortening effect (17%) of GPS persisted (GPS, 105±14ms, vs. 127±8ms at baseline and 125±10ms after recovery, p<0.05) with a trend towards being less pronounced as compared to GPS effect without H9335 (−18±6ms vs. −29±3ms, p=0.07). However, the GPS-induced CV slowing was abolished by H9335 (97±14cm/sec, vs. 103±15cm/sec at baseline and 101±16cm/sec after recovery, p=0.23). The effects of endogenous VIP were eliminated by atropine during GPS, indicating VIP release from intrinsic cardiac neurons may be mediated by muscarinic recpetors. Conclusion: Neuronally released VIP could contribute vagal effects and is primarily responsible for CV slowing during GPS. Neuronal release of VIP is likely mediated by muscarinic receptors in the intrinsic cardiac neurons.

Indexing technique has been used extensively in order to facilitate and optimize query processing in various data retrieval and storage systems. Although an index technique can be used to reduce searching cost in both horizontal and vertical dimensions, it incurs both storage and maintenance costs. Index selection has been an active research subject, and various index selection methods have been given in literature. This paper will present a framework to mine frequent query patterns to select most frequently used access paths as candidates for index selection, and a Bayesian based method will be used to select index fields from the candidate set.

Although there have been significant advancements in developing iris-based identification processes during recent years, there remains significant room for improvement. This paper presents an automatic iris recognition system including a novel approach to the iris localization and k-d tree code matching. In order to compare the k-d tree code-matching method proposed in this research, we have implement some of algorithms used in Iris recognition for the purposes of experiments and comparisons and achieved satisfactory results.

Background Vasoactive intestinal polypeptide (VIP) is released from intracardiac neurons during vagal stimulation, ischemia, and heart failure, which are associated with increased vulnerability to atrial fibrillation. VIP shortens atrial effective refractory periods in dogs. Endogenous VIP contributes to vagally mediated acceleration of atrial electric remodeling. VIP is also shown to prolong the duration of acetylcholine-induced atrial fibrillation. However, the ionic mechanisms underlying VIP effects are largely unknown.Methods and Results The effects of VIP on transmembrane ion channels were studied in canine atrial cardiomyocytes using patch-clamp techniques. VIP increased delayed rectifier K+ current and L-type calcium current but decreased the transient outward K+ current and sodium current. Optical mapping technique was used to assess effects of VIP on action potential durations (APDs) in isolated canine left atria. VIP shortened APD and slowed conduction velocity in a dose-dependent manner. Furthermore, VIP increased spatial heterogeneity of APD and conduction velocity, as assessed by the SDs of APD and conduction velocity, and atrial fibrillation inducibility.Conclusions Through its diverse effects on ion channels, VIP shortens APD with increased APD spatial heterogeneity and decreases intra-atrial conduction velocity, which may play an important role in the pathogenesis of atrial arrhythmias in scenarios where VIP release is increased.