Implantable Cardioverter Defibrillator in a Patient with Eisenmenger Syndrome after Senning Repair for Transposition of the Great Arteries

An implantation of a cardioverter-defibrillator was attempted in a 32-year-old man with atrial tachycardia, ventricular tachycardia and sinus node dysfunction. He had undergone a Senning operation and half closure of ventricular septal defect in order to correct a transposition of the great arteries. Cardiac catheterization revealed severe pulmonary hypertension and Eisenmenger syndrome. Prior knowledge of the complex cardiac anatomy obtained by magnetic resonance imaging helped in determining the suitable site for implanting the leads and planning the procedural strategy. With repletion of a large amount of saline and oral anticoagulation with warfarin, no complications related to thromboembolism occurred during a 10-month follow-up period

The Performance Test of pnCCD with FPGA-Based Operating System for a CubeSat Mission

On 17 August 2017, the LIGO/Virgo collaboration detected a signal of gravitational waves, named GW170817, associated with the merger of two neutron stars. This event was the first detection of the electromagnetic counterpart of gravitational wave events. In general, the error image region of the gravitational wave detectors ranges from a few square degrees to several hundred square degrees. To search for the origin of the gravitational waves or the energetic explosions such as the gamma-ray burst, X-ray observation covering a wide field of view with a good sensitivity is essential to achieve the goal. One of the good candidate instruments to achieve our goal is the combination of an X-ray optics called Lobster-eye optics (LEO) and a large area Si pixel imaging sensor. Furthermore, thanks to the light weight of LEO, it is possible to install on a small platform such as a CubeSat. Here, we introduce a future 3U CubeSat mission for searching the electromagnetic counterpart of gravitational waves in the soft X-ray band (0.4 ~ 10 keV) with ~arcmin localization accuracy. The pnCCD detector fabricated by PNSensor Inc. can achieve our mission requirements as an X-ray detector. To operate the pnCCD detector, we developed an FPGA-based fast readout system which is a very compact design to install on the CubeSat mission.Also, we investigate the readout noise of CAMEX, which is the readout ASIC of pnCCD. As a result, the readout noise was ~ 7.4 e-. In this paper, we report the performance of pnCCD applying our compact FPGA-based data processing system

Diacylglycerol kinase ζ inhibits myocardial atrophy and restores cardiac dysfunction in streptozotocin-induced diabetes mellitus

<p>Abstract</p> <p>Background</p> <p>Activation of the diacylglycerol (DAG)-protein kinase C (PKC) pathway has been implicated in the pathogenesis of a number of diabetic complications. Diacylglycerol kinase (DGK) converts DAG to phosphatidic acid and acts as an endogenous regulator of PKC activity. Akt/PKB is associated with a downstream insulin signaling, and PKCβ attenuates insulin-stimulated Akt phosphorylation.</p> <p>Methods and Results</p> <p>We examined transgenic mice with cardiac-specific overexpression of DGKζ (DGKζ-TG) compared to wild type (WT) mice in streptozotocin-induced (STZ, 150 mg/kg) diabetic and nondiabetic conditions. After 8 weeks, decreases in heart weight and heart weight/body weight ratio in diabetic WT mice were inhibited in DGKζ-TG mice. Echocardiography at 8 weeks after STZ-injection demonstrated that decreases in left ventricular end-diastolic diameter and fractional shortening observed in WT mice were attenuated in DGKζ-TG mice. Thinning of the interventricular septum and the posterior wall in diabetic WT hearts were blocked in DGKζ-TG mice. Reduction of transverse diameter of cardiomyocytes isolated from the left ventricle in diabetic WT mice was attenuated in DGKζ-TG mice. Cardiac fibrosis was much less in diabetic DGKζ-TG than in diabetic WT mice. Western blots showed translocation of PKCβ and δ isoforms to membrane fraction and decreased Akt/PKB phosphorylation in diabetic WT mouse hearts. However in diabetic DGKζ-TG mice, neither translocation of PKC nor changes Akt/PKB phosphorylation was observed.</p> <p>Conclusion</p> <p>DGKζ modulates intracellular signaling and improves the course of diabetic cardiomyopathy. These data may suggest that DGKζ is a new therapeutic target to prevent or reverse diabetic cardiomyopathy.</p

Association of plasma thioredoxin-1 with renal tubular damage and cardiac prognosis in patients with chronic heart failure

AbstractBackgroundThioredoxin-1 (Trx-1) is an abundant 12.5kDa redox protein expressed in almost all eukaryotic cells that protect against the development of heart failure and kidney dysfunction. Plasma Trx-1 levels are considered as a reliable marker for oxidative stress. However, it remains to be determined whether plasma Trx-1 levels can predict cardiac prognosis in patients with chronic heart failure (CHF).Methods and resultsWe measured plasma Trx-1 levels and urinary β2-microglobulin–creatinine ratio (UBCR), a marker for renal tubular damage, in 156 consecutive patients with CHF and 17 control subjects. The patients were prospectively followed for a median follow-up period of 627 days and 46 cardiac events were observed. The patients with cardiac events had significantly higher plasma Trx-1 levels and UBCR levels than the cardiac event-free patients. Multivariate Cox proportional hazard analysis revealed that an elevated Trx-1 level was independently associated with poor outcome in patients with CHF after adjustment for confounding factors (hazard ratio, 1.74; 95% confidence interval, 1.33–2.29; p<0.0001). UBCR was increased with higher plasma Trx-1 levels. Kaplan–Meier analysis demonstrated that the highest Trx-1 tertile was associated with the highest risk of cardiac events.ConclusionPlasma Trx-1 level was associated with renal tubular damage and cardiac prognosis, suggesting that it could be a useful marker to identify patients at high risk for comorbid heart failure and renal tubular damage

An Optically Dark GRB Observed by HETE-2: GRB 051022

GRB 051022 was detected at 13:07:58 on 22 October 2005 by HETE-2. The location of GRB 051022 was determined immediately by the flight localization system. This burst contains multiple pulses and has a rather long duration of about 190 seconds. The detections of candidate X-ray and radio afterglows were reported, whereas no optical afterglow was found. The optical spectroscopic observations of the host galaxy revealed the redshift z = 0.8. Using the data derived by HETE-2 observation of the prompt emission, we found the absorption N_H = 8.8 -2.9/+3.1 x 10^22 cm^-2 and the visual extinction A_V = 49 -16/+17 mag in the host galaxy. If this is the case, no detection of any optical transient would be quite reasonable. The absorption derived by the Swift XRT observations of the afterglow is fully consistent with those obtained from the early HETE-2 observation of the prompt emission. Our analysis implies an interpretation that the absorbing medium could be outside external shock at R ~ 10^16 cm, which may be a dusty molecular cloud.Comment: 6 pages, 2 figures, accepted for publication in PASJ lette

High-mobility group box 1-mediated heat shock protein beta 1 expression attenuates mitochondrial dysfunction and apoptosis

AbstractAimsApoptosis of cardiomyocytes is thought to account for doxorubicin cardiotoxicity as it contributes to loss of myocardial tissue and contractile dysfunction. Given that high-mobility group box 1 (HMGB1) is a nuclear DNA-binding protein capable of inhibiting apoptosis, we aimed to clarify the role of HMGB1 in heat shock protein beta 1 (HSPB1) expression during doxorubicin-induced cardiomyopathy.Methods and resultsMitochondrial damage, cardiomyocyte apoptosis, and cardiac dysfunction after doxorubicin administration were significantly attenuated in mice with cardiac-specific overexpression of HMGB1 (HMGB1-Tg) compared with wild type (WT) -mice. HSPB1 levels after doxorubicin administration were significantly higher in HMGB1-Tg mice than in WT mice. Transfection with HMGB1 increased the expression of HSPB1 at both the protein and mRNA levels, and HMGB1 inhibited mitochondrial dysfunction and apoptosis after exposure of cardiomyocytes to doxorubicin. HSPB1 silencing abrogated the inhibitory effect of HMGB1 on cardiomyocyte apoptosis. Doxorubicin increased the binding of HMGB1 to heat shock factor 2 and enhanced heat shock element promoter activity. Moreover, HMGB1 overexpression greatly enhanced heat shock element promoter activity. Silencing of heat shock factor 2 attenuated HMGB1-dependent HSPB1 expression and abrogated the ability of HMGB1 to suppress cleaved caspase-3 accumulation after doxorubicin stimulation.ConclusionsWe report the first in vivo and in vitro evidence that cardiac HMGB1 increases HSPB1 expression and attenuates cardiomyocyte apoptosis associated with doxorubicin-induced cardiomyopathy. Cardiac HMGB1 increases HSPB1 expression in cardiomyocytes in a heat shock factor 2-dependent manner

HETE-2 Observations of the X-Ray Flash XRF 040916

A long X-ray flash was detected and localized by the instruments aboard the High Energy Transient Explorer II (HETE-2) at 00:03:30 UT on 2004 September 16. The position was reported to the GRB Coordinates Network (GCN) approximately 2 hours after the burst. This burst consists of two peaks separated by 200 s, with durations of 110 s and 60 s. We have analyzed the energy spectra of the 1st and 2nd peaks observed with the Wide Field X-Ray Monitor (WXM) and the French Gamma Telescope (FREGATE). We discuss the origin of the 2nd peak in terms of flux variabilities and timescales. We find that it is most likely part of the prompt emission, and is explained by the long-acting engine model. This feature is similar to some bright X-ray flares detected in the early afterglow phase of bursts observed by the Swift satellite.Comment: 9 pages, 4 figures, Accepted for publication in PAS