Development of a cryogen-free sub-3 K low-temperature scanning probe microscope by remote liquefaction scheme.

We developed a new scheme for cryogen-free cooling down to sub-3 K temperature range and ultra-low vibration level. An ultra-high-vacuum cryogen-free scanning probe microscope (SPM) system was built based on the new scheme. Instead of mounting a below-decoupled cryocooler directly onto the system, the new design was realized by integrating a Gifford-McMahon cryocooler into a separate liquefying chamber, providing two-stage heat exchangers in a remote way. About 10 L of helium gas inside the gas handling system was cooled, liquefied in the liquefying chamber, and then transferred to a continuous-flow cryostat on the SPM chamber through an ∼2 m flexible helium transfer line. The exhausted helium gas from the continuous-flow cryostat was then returned to the liquefying chamber for reliquefaction. A base temperature of ∼2.84 K at the scanner sample stage and a temperature fluctuation of almost within ±0.1 mK at 4 K were achieved. The cooling curves, tunneling current noise, variable-temperature test, scanning tunneling microscopy and non-contact atomic force microscopy imaging, and first and second derivatives of I(V) spectra are characterized to verify that the performance of our cryogen-free SPM system is comparable to the bath cryostat-based low-temperature SPM system. This remote liquefaction close-cycle scheme shows conveniency to upgrade the existing bath cryostat-based SPM system, upgradeability of realizing even lower temperature down to sub-1 K range, and great compatibility of other physical environments, such as high magnetic field and optical accesses. We believe that the new scheme could also pave a way for other cryogenic applications requiring low temperature but sensitive to vibration.

Circ_0001312 Silencing Suppresses Doxorubicin-Induced Cardiotoxicity via MiR-409-3p/HMGB1 Axis.

Doxorubicin (DOX) is a potent cytotoxic chemotherapeutic agent limited in clinical application owing to its cumulative and irreversible cardiotoxicity. Circ_0001312 is highly expressed in patients with heart failure. However, it is still unclear whether circ_0001312 plays any roles in DOX-induced cardiotoxicity.Human AC16 cardiomyocytes in functional group were stimulated with DOX. The levels of genes and proteins were detected by qRT-PCR and western blotting. The proliferation, apoptosis, as well as inflammatory and oxidative injury in cardiomyocytes were investigated. Dual-luciferase reporter, RNA immunoprecipitation, and pull-down assays were utilized to confirm the binding between miR-409-3p and circ_0001312 or HMGB1 (high-mobility group box 1). Exosomes were isolated by using the commercial kit and identified by transmission electron microscopy (TEM) and nanoparticle-tracking analysis (NTA).DOX impaired cardiomyocyte proliferation and induced apoptotic, inflammatory, and oxidative injury in cells. Furthermore, it promoted circ_0001312 expression, and the knockdown of circ_0001312 could reverse DOX-evoked cardiomyocyte injury. In terms of mechanics, circ_0001312 bound competitively to miR-409-3p to up-regulate HMGB1, which was a target of miR-409-3p. DOX decreased the miR-409-3p but increased the HMGB1 expression in cardiomyocytes. Functionally, miR-409-3p inhibition attenuated the protective action of circ_0001312 silencing on cardiomyocytes under DOX treatment. Moreover, miR-409-3p could abate DOX-evoked apoptosis, and inflammation and oxidative stress in cardiomyocytes, and these effects were counteracted by HMGB1 overexpression. In addition, circ_0001312 was secreted by exosomes and could be transmitted via exosomes.Circ_0001312 reversed the cytotoxic effects mediated by DOX on cardiomyocytes via the miR-409-3p/HMGB1 axis. Besides, it was released to the extracellular space by exosomes.

CircSAMD4A aggravates H/R-induced cardiomyocyte apoptosis and inflammatory response by sponging miR-138-5p.

Hypoxia/reoxygenation (H/R)-induced myocardial cell injury is the main cause of acute myocardial infarction (AMI). Many proofs show that circular RNA plays an important role in the development of AMI. The purpose of this study was to investigate the role of circSAMD4A in H/R-induced myocardial injury. The levels of circular SAMD4A (circSAMD4A) were detected in the heart tissues of AMI mice and H/R-induced H9C2 cells, and the circSAMD4A was suppressed in AMI mice and H/R-induced H9C2 cells to investigate its' function in AMI. The levels of circSAMD4A and miR-138-5p were detected by real-time quantitative PCR, and MTT assay was used to detect cell viability. TUNEL analysis and Annexin V-FITC were used to determine apoptosis. The expression of Bcl-2 and Bax proteins was detected by Western blot. IL-1ß, TNF-α and IL-6 were detected by ELISA kits. The study found that the levels of circSAMD4A were up-regulated after H/R induction and inhibition of circSAMD4A expression would reduce the H/R-induced apoptosis and inflammation. MiR-138-5p was down-regulated in H/R-induced H9C2 cells. circSAMD4A was a targeted regulator of miR-138-5p. CircSAMD4A inhibited the expression of miR-138-5p to promote H/R-induced myocardial cell injury in vitro and vivo. In conclusion, CircSAMD4A can sponge miR-138-5p to promote H/R-induced apoptosis and inflammatory response.

A time-shared switching scheme designed for multi-probe scanning tunneling microscope.

We report the design of a time-shared switching scheme, aiming to realize the manipulation and working modes (imaging mode and transport measurement mode) switching between multiple scanning tunneling microscope (STM) probes one by one with a shared STM control system (STM CS) and an electrical transport characterization system. This scheme comprises three types of switch units, switchable preamplifiers (SWPAs), high voltage amplifiers, and a main control unit. Together with the home-made software kit providing the graphical user interface, this scheme achieves a seamless switching process between different STM probes. Compared with the conventional scheme using multiple independent STM CSs, this scheme possesses more compatibility, flexibility, and expansibility for lower cost. The overall architecture and technique issues are discussed in detail. The performances of the system are demonstrated, including the millimeter scale moving range and atomic scale resolution of a single STM probe, safely approached multiple STM probes beyond the resolution of the optical microscope (1.1 µm), qualified STM imaging, and accurate electrical transport characterization. The combinational technique of imaging and transport characterization is also shown, which is supported by SWPA switches with ultra-high open circuit resistance (909 TΩ). These successful experiments prove the effectiveness and the usefulness of the scheme. In addition, the scheme can be easily upgraded with more different functions and numbers of probe arrays, thus opening a new way to build an extremely integrated and high throughput characterization platform.

Atomically sharp interface enabled ultrahigh-speed non-volatile memory devices.

The development of high-performance memory devices has played a key role in the innovation of modern electronics. Non-volatile memory devices have manifested high capacity and mechanical reliability as a mainstream technology; however, their performance has been hampered by low extinction ratio and slow operational speed. Despite substantial efforts to improve these characteristics, typical write times of hundreds of micro- or milliseconds remain a few orders of magnitude longer than that of their volatile counterparts. Here we demonstrate non-volatile, floating-gate memory devices based on van der Waals heterostructures with atomically sharp interfaces between different functional elements, achieving ultrahigh-speed programming/erasing operations in the range of nanoseconds with extinction ratio up to 1010. This enhanced performance enables new device capabilities such as multi-bit storage, thus opening up applications in the realm of modern nanoelectronics and offering future fabrication guidelines for device scale up.

TMAO: a potential mediator of clopidogrel resistance.

Trimethylamine-N-oxide (TMAO) can activate platelets and increase thrombosis risk in clinical and experimental models. Meanwhile, the patients with coronary artery disease have higher serum TMAO level. However, it remains unknown whether Clopidogrel Resistance (CR) could be attributed to TMAO. The present study aimed investigate the effects of TMAO on clopidogrel in ischemia and reperfusion (IR) model in rats. Clopidogrel could (1) promote the production of platelets, induce an increase in the platelet-larger cell ratio; (2) prolong the tail bleeding time; (3) reduce platelet aggregation function, induced by ADP, and alleviate myocardial thrombus burden. TMAO could partially offset the effects of clopidogrel and induce CR. Thus, the present study demonstrated that circulating TMAO could reduce the inhibitory effects of clopidogrel on platelet aggregation. TMAO may be a potential mediator of clopidogrel resistance.

Localized spin-orbit polaron in magnetic Weyl semimetal Co3Sn2S2.

The kagome lattice Co3Sn2S2 exhibits the quintessential topological phenomena of a magnetic Weyl semimetal such as the chiral anomaly and Fermi-arc surface states. Probing its magnetic properties is crucial for understanding this correlated topological state. Here, using spin-polarized scanning tunneling microscopy/spectroscopy (STM/S) and non-contact atomic force microscopy (nc-AFM) combined with first-principle calculations, we report the discovery of localized spin-orbit polarons (SOPs) with three-fold rotation symmetry nucleated around single S-vacancies in Co3Sn2S2. The SOPs carry a magnetic moment and a large diamagnetic orbital magnetization of a possible topological origin associated relating to the diamagnetic circulating current around the S-vacancy. Appreciable magneto-elastic coupling of the SOP is detected by nc-AFM and STM. Our findings suggest that the SOPs can enhance magnetism and more robust time-reversal-symmetry-breaking topological phenomena. Controlled engineering of the SOPs may pave the way toward practical applications in functional quantum devices.

Ferroelectric-Gated InSe Photodetectors with High On/Off Ratios and Photoresponsivity.

Indium selenide (InSe) has a high electron mobility and tunable direct band gap, enabling its potential applications to electronic and optoelectronic devices. Here, we report the fabrication of InSe photodetectors with high on/off ratios and ultrahigh photoresponsivity, using ferroelectric poly(vinylidene fluoride-trifluoroethylene) (P(VDF-TrFE)) copolymer films as the top-gate dielectric. Benefiting from the successful suppression of the dark current down to ∼10-14A in the InSe channel by tuning the three different polarization states in ferroelectric P(VDF-TrFE) and improved interface properties using h-BN as a substrate, the ferroelectric-gated InSe photodetectors show a high on/off ratio of over 108, a high photoresponsivity up to 14 250 AW-1, a high detectivity up to 1.63 × 1013 Jones, and a fast response time of 600 µs even at zero-gate voltage. The present results highlight the role of ferroelectric P(VDF-TrFE) in tuning the carrier transport of InSe and may provide an avenue for the development of InSe-based photodetectors.

Wrinkle-induced highly conductive channels in graphene on SiO2/Si substrates.

A graphene wrinkle is a quasi-one-dimensional structure and can alter the intrinsic physical and chemical activity, modify the band structure and introduce transport anisotropy in graphene thin films. However, the quasi-one-dimensional electrical transport contribution of wrinkles to the whole graphene films compared to that of the two-dimensional flat graphene nearby has still been elusive. Here, we report measurements of relatively high conductivity in micrometer-wide graphene wrinkles on SiO2/Si substrates using an ultrahigh vacuum (UHV) four-probe scanning tunneling microscope. Combining the experimental results with resistor network simulations, the wrinkle conductivity at the charge neutrality point shows a much higher conductivity up to ∼33.6 times compared to that of the flat monolayer region. The high conductivity can be attributed not only to the wrinkled multilayer structure but also to the large strain gradients located mainly in the boundary area. This method can also be extended to evaluate the electrical-transport properties of wrinkled structures in other two-dimensional materials.

PTPN2 negatively regulates macrophage inflammation in atherosclerosis.

Atherosclerosis is the main cause of cardiovascular disease. Systemic inflammation is one important characteristic in atherosclerosis. Pro-inflammatory macrophages can secrete inflammatory factors and promote the inflammation of atherosclerosis. It has a great value for the treatment of atherosclerosis by inhibiting the release of inflammatory factors in macrophages. However, the detailed mechanism of this process is still unclear. In this study, we constructed an APOE-/- mice model of atherosclerosis to research the molecular mechanism of atherosclerosis. Protein tyrosine phosphatase non-receptor type 2 (PTPN2), an anti-inflammatory gene, was dramatically decreased in inflammatory mice. Deletion of PTPN2 could significantly induce monocytes toward M1 phenotype of macrophages, enhance the secretion of IL-12 and IL-1, and promote cell proliferation, invasion and metastasis. Mechanism research showed that PTPN2-mediated p65/p38/STAT3 de-phosphorylation could block the process of macrophage inflammation. In vivo experiments showed that PTPN2 may effectively inhibit the inflammatory response during atherosclerosis. In conclusion, we uncovered the negative role of PTPN2 in the occurrence of atherosclerosis, and this study provides a new potential target for atherosclerosis treatment.

Observation of the Kondo Effect in Multilayer Single-Crystalline VTe2 Nanoplates.

We report the chemical vapor deposition (CVD) growth, characterization, and low-temperature magnetotransport of 1T phase multilayer single-crystalline VTe2 nanoplates. The transport studies reveal that no sign of intrinsic long-range ferromagnetism but localized magnetic moments exist in the individual multilayer metallic VTe2 nanoplates. The localized moments give rise to the Kondo effect, evidenced by logarithmical increment of resistivity with decreasing temperature and negative magnetoresistance (NMR) regardless of the direction of magnetic field at temperatures below the resistivity minimum. The low-temperature resistivity upturn is well described by the Hamann equation, and the NMR at different temperatures, a manifestation of the magnetization of the localized spins, is well fitted to a Brillouin function for S = 1/2. Density functional theory calculations reveal that the localized magnetic moments mainly come from the interstitial vanadium ions in the VTe2 nanoplates. Our results will shed light on the study of magnetic properties, strong correlation, and many-body physics in two-dimensional metallic transition metal dichalcogenides.

Quasi-2D Transport and Weak Antilocalization Effect in Few-layered VSe2.

With strong spin-orbit coupling (SOC), ultrathin two-dimensional (2D) transitional metal chalcogenides (TMDs) are predicted to exhibit weak antilocalization (WAL) effect at low temperatures. The observation of WAL effect in VSe2 is challenging due to the relative weak SOC and three-dimensional (3D) transport nature in thick VSe2. Here, we report on the observation of quasi-2D transport and WAL effect in sublimed-salt-assisted low-temperature chemical vapor deposition (CVD) grown few-layered high-quality VSe2 nanosheets. The WAL magnitudes in magnetoconductance can be perfectly fitted by the 2D Hikami-Larkin-Nagaoka (HLN) equation in the presence of strong SOC, by which the spin-orbit scattering length lSO and phase coherence length lϕ have been extracted. The phase coherence length lϕ shows a power law dependence with temperature, lϕ∼ T-1/2, revealing an electron-electron interaction-dominated dephasing mechanism. Such sublimed-salt-assisted growth of high-quality few-layered VSe2 and the observation of WAL pave the way for future spintronic and valleytronic applications.

Iron-load exacerbates the severity of atherosclerosis via inducing inflammation and enhancing the glycolysis in macrophages.

Atherosclerosis is still the major cause of morbidity and mortality all over the world. Recently, it has been reported increased levels of tissue iron increase the risk of atherosclerosis. However, the detailed mechanism of iron-induced atherosclerosis progression is barely known. Here, we used apoE-deficient mice models to investigate the effects of low iron diet (<0 mg iron carbonyl/kg), high iron diet (25,000 mg iron carbonyl/kg) on atherosclerosis in vivo. As exhibited, we observed that CD68 was significant enriched by high iron diet in apoE-deficient mice. In addition, transforming growth factor ß, tumor necrosis factor α, interleukin 6 (IL-6), IL-23, IL-10, and IL-1ß levels were also greatly induced by high iron diet. Then, we found that the iron load promoted the inflammation response in macrophages. Moreover, macrophage polarization is a process by which macrophage can express various functional programs in activating macrophages. Here, we observed that iron-load macrophages were polarized toward a proinflammatory macrophage phenotype. The polarization of M1 macrophage was promoted by ferric ammonium citrate (FAC) in bone marrow derived macrophages (BMDMs). Furthermore, ECAR and cellular OCR in BMDM with or without FAC was examined. As shown, BMDM indicated with 50 µM FAC showed a significant increase in basic state and maximal ECAR in contrast to the control group. However, there was no significant difference in OCR. This indicated that the glycolysis was involved in the polarization of M1 macrophage triggered by iron-load. In conclusion, we indicated that the iron load exacerbates the progression of atherosclerosis via inducing inflammation and enhancing glycolysis in macrophages.

Sub-10 nm stable graphene quantum dots embedded in hexagonal boron nitride.

Graphene quantum dots (GQDs), a zero-dimensional material system with distinct physical properties, have great potential in the applications of photonics, electronics, photovoltaics, and quantum information. In particular, GQDs are promising candidates for quantum computing. In principle, a sub-10 nm size is required for GQDs to present the intrinsic quantum properties. However, with such an extreme size, GQDs have predominant edges with lots of active dangling bonds and thus are not stable. Satisfying the demands of both quantum size and stability is therefore of great challenge in the design of GQDs. Herein we demonstrate the fabrication of sub-10 nm stable GQD arrays by embedding GQDs into large-bandgap hexagonal boron nitride (h-BN). With this method, the dangling bonds of GQDs were passivated by the surrounding h-BN lattice to ensure high stability, meanwhile maintaining their intrinsic quantum properties. The sub-10 nm nanopore array was first milled in h-BN using an advanced high-resolution helium ion microscope and then GQDs were directly grown in them through the chemical vapour deposition process. Stability analysis proved that the embedded GQDs show negligible property decay after baking at 100 °C in air for 100 days. The success in preparing sub-10 nm stable GQD arrays will promote the physical exploration and potential applications of this unique zero-dimensional in-plane quantum material.

LncRNA UCA1 sponges miR-206 to exacerbate oxidative stress and apoptosis induced by ox-LDL in human macrophages.

Long noncoding RNA UCA1 has exerted a significant effect in cardiovascular disease. The biological role of UCA1 in atherosclerosis is unclear. Our study was to identify the potential mechanisms in the progression of atherosclerosis. Here, we observed that ox-LDL increased UCA1 expression greatly in THP-1 cells. Knockdown of UCA1 greatly inhibited CD36 expression, a crucial biomarker in atherosclerosis. Meanwhile, 20 µg/ml ox-LDL induced foam cell formation, which can be reversed by downregulation of UCA1. In addition, TC and TG levels induced by ox-LDL was rescued by UCA1 small interfering RNA. Accumulating studies have indicated that oxidative stress contributes to atherosclerosis progression. Here, we also found that reactive oxygen species, MDA, and THP-1 cell apoptosis were restrained by decreased of UCA1 with an increase of the superoxide dismutase activity. Moreover, miR-206 was predicted as a target of UCA1 and knockdown of UCA1 was able to repress miR-206 expression. Furthermore, overexpression of miR-206 inhibited oxidative stress process and it was reversed by UCA1 upregulation in vitro. In conclusion, we indicated that UCA1 sponged miR-206 to exacerbate atherosclerosis events induced by ox-LDL in THP-1 cells.

Selective ablation of atrial ganglionated plexus attenuates vasovagal reflex in a canine model.

BACKGROUND: Atrial ganglionated plexus (GP) ablation was proved to have therapeutic effects on vasovagal syncope. The study aimed to investigate whether selective ablation of only right anterior GP (ARGP) and right inferior GP (IRGP) was effective in a canine model of vasovagal syncope. METHODS: Seventeen mongrel dogs were divided into control (N = 10) and ablation group (N = 7). Bilateral thoracotomy was performed at the fourth intercostal space and ARGP and IRGP were ablated in the ablation group. A bolus of veratridine (15 ug/kg) was injected into the left atrium to induce vasovagal reflex. Surface electrocardiogram and blood pressure (BP) were continuously monitored. Heart rate (HR) variability was calculated to represent cardiac autonomic tone. RESULTS: Veratridine injection induced vasovagal reflex in all dogs. HR decreased from 149 ± 17 to 89 ± 33 beats/min (P < 0.001) in the control group, while in the ablation group HR decreased from 141 ± 35 to 125 ± 34 beats/min (P = 0.032). The postveratridine HR in the ablation group was significantly higher than that in the control group (P = 0.045). A significantly less intense HR decrease was observed in the ablation group compared with control (-17 ± 16 vs -61 ± 34 beats/min, P = 0.006). Significant BP decreases were induced in both the groups (all P < 0.01), while no evident differences in postveratridine BP and the extent of BP decreases were found between the groups. HR variability revealed significant decrease in cardiac vagal tone after ablation [high-frequency power, 0.50 (0.17-1.05) vs 6.28 (0.68-8.99) ms2 , P = 0.005]. CONCLUSIONS: Selective ablation of ARGP + IRGP weakened cardiac parasympathetic control and significantly attenuated the cardioinhibitory response in an animal model of vasovagal reflex. This ablation strategy might be effective for vasovagal syncope with evident cardioinhibitory response.

A low-temperature scanning probe microscopy system with molecular beam epitaxy and optical access.

A low-temperature ultra-high vacuum scanning probe microscopy (SPM) system with molecular beam epitaxy (MBE) capability and optical access was conceived, built, and tested in our lab. The design of the whole system is discussed here, with special emphasis on some critical parts. The SPM scanner head takes a modified Pan-type design with improved rigidity and compatible configuration to optical access and can accommodate both scanning tunneling microscope (STM) tips and tuning-fork based qPlus sensors. In the system, the scanner head is enclosed by a double-layer cold room under a bath type cryostat. Two piezo-actuated focus-lens stages are mounted on both sides of the cold room to couple light in and out. The optical design ensures the system's forward compatibility to the development of photo-assisted STM techniques. To test the system's performance, we conducted STM and spectroscopy studies. The herringbone reconstruction and atomic structure of an Au(111) surface were clearly resolved. The dI/dV spectra of an Au(111) surface were obtained at 5 K. In addition, a periodic 2D tellurium (Te) structure was grown on the Au(111) surface using MBE and the atomic structure is clearly resolved by using STM.

Inhibition of autophagy via activation of PI3K/Akt/mTOR pathway contributes to the protection of hesperidin against myocardial ischemia/reperfusion injury.

Hesperidin has been reported to attenuate myocardial ischemia/reperfusion (I/R) injury; however, its effect on autophagy during myocardial I/R and the underlying mechanism remains unknown. The present study aimed to investigate whether hesperidin inhibited I/R­induced excessive myocardial autophagy through activating the phosphatidylinositol 3­kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway. Male adult rats were pretreated with hesperidin for a total of 3 days prior to ischemia in the absence or presence of LY294002, a PI3K inhibitor, and then subjected to ischemia for 30 min followed by reperfusion for 4 h. Myocardial infarct size was measured by Evans blue/triphenyltetrazolium chloride staining. Hematoxylin and eosin staining was used for observing the histological changes in the heart, and the serum levels of creatine kinase­MB (CK­MB) and cardiac troponin I (cTnI) were measured by enzyme­linked immunosorbent assay. Additionally, the protein levels of light chain (LC) 3Ⅱ, Beclin1, phosphorylated (p)­mTOR, p­Akt and p­PI3K were determined by western blot analysis. Hesperidin pretreatment significantly decreased the myocardial infarct size, myocardial damage and serum levels of CK­MB and cTnI. Furthermore, the expression levels of LC3Ⅱ and Beclin1 were significantly downregulated and the expression levels of p­mTOR, p­Akt and p­PI3K were markedly upregulated by hesperidin. However, the aforementioned effects as a result of hesperidin were significantly reversed by the presence of LY294002. These results demonstrated that hesperidin reduced myocardial I/R injury by suppressing excessive autophagy. Activation of the PI3K/Akt/mTOR pathway contributed to the inhibitory effect of hesperidin on excessive autophagy.

Selective ablation of the ligament of Marshall reduces ischemia and reperfusion-induced ventricular arrhythmias.

Cardiac sympathetic tone overdrive is a key mechanism of arrhythmia. Cardiac sympathetic nerves denervation, such as LSG ablation or renal sympathetic denervation, suppressed both the prevalence of VAs and the incidence of SCD. Accumulating evidence demonstrates the ligament of Marshall (LOM) is a key component of the sympathetic conduit between the left stellate ganglion (LSG) and the ventricles. The present study aimed to investigate the roles of the distal segment of LOM (LOMLSPV) denervation in ischemia and reperfusion (IR)-induced VAs, and compared that LSG denervation. Thirty-three canines were randomly divided into group 1 (IR group, n = 11), group 2 (LOMLSPV Denervation + IR, n = 9), and group 3 (LSG Denervation + IR, n = 13). Hematoxylin-Eosin (HE) and Immunohistochemistry staining revealed that LOMLSPV contained bundles of sympathetic but not parasympathetic nerves. IR increased the cardiac sympathetic tone [serum concentrations of noradrenaline (NE) and epinephrine (E)] and induced the prevalence of VAs [ventricular premature beat (VPB), salvo of VPB, ventricular tachycardia (VT), VT duration (VTD) and ventricular fibrillation (VF)]. Both LOMLSPV denervation and LSG denervation could reduce the cardiac sympathetic tone in Baseline (BS) [heart rate variability (HRV)]. Compared with group 1, LOMLSPV denervation and LSG denervation similarly reduced sympathetic tone [NE (1.39±0.068 ng/ml in group 2, 1.29±0.081 ng/ml in group 3 vs 2.32±0.17 ng/ml in group 1, P<0.05) and E (114.64±9.22 pg/ml in group 2, 112.60±9.69 pg/ml in group 3 vs 166.18±15.78 pg/ml in group 1, P<0.05),] and VAs [VT (0±3.00 in group 2, 0±1.75 in group 3 vs 8.00±11.00 in group 1, P<0.05) and VTD (0 ± 4 s in group 2, 0±0.88s in group 3 vs 10.0 ± 22.00s in group 1, P<0.05)] after 2h reperfusion. These findings indicated LOMLSPV denervation reduced the prevalence of VT by suppressing SNS activity. These effects are comparable to those of LSG denervation. In myocardial IR, the anti-arrhythmic effects of LOMLSPV Denervation may be related to the inhibition of the expression of NE and E.

Selective ablation of the ligament of Marshall attenuates atrial electrical remodeling in a short-term rapid atrial pacing canine model.

INTRODUCTION: Cardiac sympathetic activation facilitates atrial electrical remodeling during atrial fibrillation (AF). Selective ablation of the distal part of the ligament of Marshall (LOMLSPV ) could decrease cardiac sympathetic innervation. This study aimed to investigate the effects of LOMLSPV ablation on atrial electrical remodeling in a short-term rapid atrial pacing (RAP) model. METHODS: In 16 anesthetized dogs, 6 hours of RAP (20 Hz, 2 × threshold) was delivered before LOMLSPV ablation (group 1, N  =  8) or after (group 2, N  =  8). Heart rate variability (HRV), serum norepinephrine (NE), atrial electrophysiological indices were analyzed. Six times of burst pacing (20 Hz, 2 × threshold, lasting for 5 seconds, were performed to induce AF, the number of episodes and the duration of AF were compared. RESULTS: LOMLSPV ablation decreased sympathetic indices of HRV and serum NE. Atrial effective refractory period (ERP) was shortened during RAP in both groups with higher reduction degrees in group 1. In group 1, the shortening of atrial ERP, elevating of ERP dispersion and sum of window of vulnerability (ΣWOV), facilitating of AF induced by RAP were subsequently reversed by LOMLSPV ablation. In group 2, LOMLSPV ablation prolonged atrial ERP, decreased ΣWOV, eliminated AF induction. The subsequent RAP failed to alter these indices. Histological studies showed abundant sympathetic nerve fibers in LOMLSPV . CONCLUSION: LOMLSPV ablation could inhibit atrial electrical remodeling during short-term RAP by reducing the cardiac sympathetic activity. LOMLSPV may be a potential target in AF ablation, especially in patients with highly cardiac sympathetic activation or atrial electrical remodeling.