SPADExp: A photoemission angular distribution simulator directly linked to first-principles calculations

We develop a software package SPADExp (simulator of photoemission angular distribution for experiments) to calculate the photoemission angular distribution (PAD), which is the momentum dependence of spectrum intensity in angle-resolved photoemission spectroscopy (ARPES). The software can directly load the output of the first-principles software package OpenMX, so users do not need to construct tight-binding models as previous studies did for PAD calculations. As a result, we can calculate the PADs of large systems such as quasicrystals and slab systems. We calculate the PADs of sublattice systems (graphene and graphite) to reproduce characteristic intensity distributions, which ARPES has experimentally observed. After that, we investigate twisted bilayer graphene, a quasicrystal showing 12-fold rotational symmetric spectra in ARPES, and the surface states of the topological insulator $\mathrm{Bi}_2\mathrm{Se}_3$. Our calculations show good agreement with previous ARPES measurements, showing the correctness of our calculation software and further potential to investigate the photoemission spectra of novel quantum materials.Comment: 19 pages, 5 figures, Software has been developed in https://github.com/Hiroaki-Tanaka-0606/SPADEx

Hydrophobic Silicone Elastomer Chamber for Recording Trajectories of Motile Porcine Sperms without Adsorption

Motile porcine sperms adhere to hydrophilic materials such as glass and plastics. The adsorption of sperms to a hydrophobic poly(dimethylsiloxane) (PDMS) membrane is less compared with that to glass. We investigated the linear velocity (LV) and amplitude of lateral head displacement (ALHD) of motile porcine sperm on glass and PDMS preparations using computer-assisted sperm analysis (CASA). Significant decreases were observed in the 15-min LV (P<0.05) and ALHD (P<0.05) in motile porcine sperm on glass preparations compared with those on PDMS preparations. These differences were due to adsorption of the head and/or neck to hydrophilic substrates. Because of the elasticity of PDMS, we propose that a PDMS membrane should be used for CASA. To investigate the dynamics of motile porcine sperms with microfluidics, we do not recommend plasma treatment to bond PDMS and glass in the microchannel preparation; instead, we suggest that a PDMS molding process without plasma treatment be used for preparation of microfluidic channels

Brachial Artery Dissection Caused by Closed Elbow Dislocation in a Snowboarder: A Case Report and Review of Literature

This report describes a rare case of brachial artery dissection associated with closed elbow dislocation caused by a snowboarding injury. After peripheral ischaemic findings in the right upper extremity were confirmed, urgent duplex-sonography was performed to diagnose the brachial artery injury. Urgent revascularisation surgery was promptly performed, and arterial dissection was diagnosed by intraoperative findings, in which the adventitia of the brachial artery was intact and the intima was disrupted. In this case, because there was no golden time window before undertaking urgent revascularisation surgery, duplex-sonography was very useful for making an emergency diagnosis. To diagnose arterial dissection, because the adventitia of the brachial artery is intact, it is necessary to perform arteriotomy to identify intimal disruption in the brachial artery. When diagnosing traumatic elbow dislocation, it is important to suspect arterial dissection

Duration of Postoperative Fever as a Simple and Useful Prognostic Indicator in Gastric Cancer Patients

[Background] Postoperative inflammation is associated with cancer progression in several cancers. However, the prognostic significance of postoperative fever remains unclear in gastric cancer patients. [Methods] We enrolled 442 patients with a histopathological diagnosis of gastric adenocarcinoma who underwent curative surgery. [Results] The mean duration of postoperative fever ≥ 37°C was 8.7 days (range: 0–186 days) and significantly longer in patients with advanced gastric cancer, venous invasion, and open or total gastrectomy vs. patients with early gastric cancer (P = 0.0072), no venous invasion (P = 0.025), laparoscopic gastrectomy (P = 0.027), and either proximal or distal partial gastrectomy (P = 0.0015). Five-year overall survival rates were 69.5% vs. 83.6% in the prolonged postoperative fever group (≥ 6 days of ≥ 37°C) vs. the nonprolonged group (< 6 days of ≥ 37°C), respectively (P = 0.0008). In patients without Clavien-Dindo classification postoperative infectious complications grade ≥ 2, 5-year overall survival was 69.7% vs. 84.0% in patients with prolonged postoperative fever vs. those without, respectively (P = 0.0067). Five-year disease-specific survival was 85.9% vs. 93.1% in patients with prolonged fever vs. those without, respectively (P = 0.041). Multivariate analysis indicated that postoperative fever was an independent prognostic indicator. [Conclusion] Postoperative fever ≥ 37°C duration may be useful in predicting prognosis in gastric cancer patients

Activated Protein Kinase C Attenuates Ca2+ Overloading and Reoxygenation Hypercontracture in Isolated Rat Cardiomyocytes following Chemical Hypoxia

The aims of this study were i) to test the effects of protein kinase C (PKC) activation on the intracellular Ca2+ concentration of rat cardiomyocytes during chemical hypoxia-reoxygenation, ii) to determine the contribution of the sarcoplasmic reticulum (SR) and the Na+-Ca2+ exchange on the regulation of intracellular Ca2+ following PKC activation and iii) to test the role of PKC-dependent intracellular pH changes in intracellular Ca2+ regulation. We used the isolated adult rat cardiomyocyte perfusion model. Cardiomyocytes were loaded with the Ca2+-fluorescent probe Fluo-3 and the pH-fluorescent probe SNARF1. Cells were subjected to 50 min of glucose-free and NaCN chemical hypoxia followed by 30 min of simulated reoxygenation. The activation of PKC significantly inhibited the hypoxia-induced increase of Fluo-3 fluorescent intensity (control; 692 ± 100% and activated PKC; 322 ± 43%: P < 0.05). This inhibitory effect was not affected by the inhibition of the SR Ca2+ uptake induced by thapsigargin, but was cancelled by the inhibition of the Na+-Ca2+ exchange with dichlorobenzamil (thapsigargin 337 ± 47%; dichlorobenzamil 609 ± 100%). PKC activation also attenuated the decrease in intracellular pH during chemical hypoxia, even in the presence of the Na+-H+ exchange inhibitor amiloride (control; 6.54 ± 0.02, PKC; 6.72 ± 0.03, PKC + amiloride; 6.73 ± 0.03). We concluded that the PKC attenuation of Ca2+ overloading to rat cardiomyocytes during chemical hypoxia-reoxygenation does not depend on the Ca2+ uptake by the SR, but does require a Na+-Ca2+ exchange. Since PKC attenuated the increasing intracellular H+ during chemical hypoxia, a low H+ concentration may be important for the maintenance of Ca2+ extrusion via the Na+-Ca2+ exchange

Induction of Apoptosis of Rat Neonatal Cardiomyocytes by Chemical Ischemia and Reoxygenation: The Role of Phosphatidylserine

Ischemia/reperfusion injury plays a crucial role in the induction of the cell death of myocytes. The precise mechanism of the cell death, however, has not been elucidated enough. This study examined the cell death of rat neonatal myocytes induced by chemical ischemia and reoxygenation with an in vitro model, in terms of apoptosis, and the role of phosphatidylserine, which is recognized with annexin V. Chemical ischemia and reoxygenation were conducted on the cultured myocytes obtained from 1- or 2-day-old Wistar rats. The cells were divided into 4 groups exposed to chemical ischemia for 9 h (Group A), 18 h (Group B) and 24 h (Group C) and one group not exposed to chemical ischemia (Control Group). DNA ladder formation on agarose gel electrophoresis was noted in Groups B and C followed by reoxygenation, but not in Group A, as well as all 4 groups without reoxygenation. There were cells positive to terminal deoxynucleotidyl transferase-mediated dUDP-biotin nick end labeling in all 3 groups except for the Control Group; after reoxygenation, the number of cells became larger in Groups B and C than in Group A. Flow cytometry revealed that annexin V-positive cells were 1.15 ± 0.82% in the Control Group, 4.07 ± 3.8% in Group A without reoxygenation and 15.5 ± 6.3% in Group A after 30-min reoxygenation, respectively; the value was significantly higher in the latter than the former two (P < 0.01). Although 18-h and 24-h ischemia increased the annexin V-positive cells, reoxygenation did not alter the number of cells in Groups B and C. These results indicate that i) chemical ischemia followed by reoxygenation variably induces apoptosis of rat myocytes, ii) long-term ischemia causes phosphatidylserine translocation on the cell surface membrane, regardless of reoxygenation and iii) mild ischemia necessitates reoxygenation to translocate phosphatidylserine, which might play a crucial role in the initiation of apoptosis of the myocytes