Noninvasive Positive Pressure Ventilation against Reperfusion Pulmonary Edema following Percutaneous Transluminal Pulmonary Angioplasty

A 69-year-old man with chronic thromboembolic pulmonary hypertension (CTEPH) was on amblatory oxygen inhalation therapy (3 L/min) and scheduled for percutaneous transluminal pulmonary angioplasty (PTPA). The patient's New York Heart Association functional status was class III with recent worsening of dyspnea and apparent leg edema. Transthoracic echocardiography revealed right ventricular enlargement with mean pulmonary artery pressure of 42 mmHg. After PTPA, he was complicated with postoperative reperfusion pulmonary edema, and noninvasive positive pressure ventilation (NPPV) was applied immediately. Hypoxemia was successfully treated with 15 days of NPPV. Although mean pulmonary artery pressure was unchanged, his brain natriuretic peptide level decreased from preoperative 390.3 to postoperative 44.3 pg/dL. In addition, total pulmonary resistance decreased from preoperative 18 to postoperative 9.6 wood unit·m2. The patient was discharged on day 25 with SpO2 of 95% on 5 L/min of oxygen inhalation. Because pulmonary edema is a postsurgical life-threatening complication following PTPA, application of NPPV should be considered

The effect of post-irradiation tumor oxygenation status on recovery from radiation-induced damage in vivo: With reference to that in quiescent cell populations

Purpose To elucidate the effect of tumor oxygenation status on recovery from damage following γ-ray or accelerated carbon ion irradiation in vivo, including in quiescent (Q) cells. Methods SCC VII tumor-bearing mice were continuously given 5-bromo-2′-deoxyuridine (BrdU) to label all proliferating (P) cells. They received γ-ray or accelerated carbon ion irradiation with or without tumor clamping for inducing hypoxia. Immediately after irradiation, cells from some tumors were isolated, or acute hypoxia-releasing nicotinamide was loaded to the tumor-bearing mice. For 9 h after irradiation, some tumors were kept aerobic or hypoxic. Then isolated tumor cells were incubated with a cytokinesis blocker. The response of Q cells was assessed in terms of the micronucleus frequency using immunofluorescence staining for BrdU. That of the total (=P + Q) tumor cells was determined from BrdU non-treated tumors. Results Clearer recovery in Q cells than total cells and after aerobic than hypoxic γ-ray irradiation was efficiently suppressed with carbon ion beams. Inhibition of recovery through keeping irradiated tumors hypoxic after irradiation and promotion of recovery by nicotinamide loading were observed more clearly with γ-rays, after aerobic irradiation and in total cells than with carbon ion beams, after hypoxic irradiation and in Q cells, respectively. Conclusions Tumor oxygenation status following irradiation can manipulate recovery from radiation-induced damage, especially after aerobic γ-ray irradiation in total cells. Carbon ion beams are promising because of their efficient suppression of the recovery

Generating Ampicillin-Level Antimicrobial Peptides with Activity-Aware Generative Adversarial Networks

Antimicrobial peptides are a potential solution to the threat of multidrug-resistant bacterial pathogens. Recently, deep generative models including generative adversarial networks (GANs) have been shown to be capable of designing new antimicrobial peptides. Intuitively, a GAN controls the probability distribution of generated sequences to cover active peptides as much as possible. This paper presents a peptide-specialized model called PepGAN that takes the balance between covering active peptides anddodging non-active peptides. As a result, PepGAN has superior statistical fidelity with respect to physicochemical descriptors including charge, hydrophobicity and weight. Top six peptides were synthesized and one of them was confirmed to be highly antimicrobial. The minimum inhibitory concentration was 3.1μg/mL, indicating that the peptide is twice as strong as ampicillin.</p

The Effect of p53 Status of Tumor Cells on Radiosensitivity of Irradiated Tumors With Carbon-Ion Beams Compared With γ-Rays or Reactor Neutron Beams

Background: The aim of the study was to clarify the effect of p53 status of tumor cells on radiosensitivity of solid tumors following accelerated carbon-ion beam irradiation compared with γ-rays or reactor neutron beams, referring to the response of intratumor quiescent (Q) cells. Methods: Human head and neck squamous cell carcinoma cells transfected with mutant TP53 (SAS/mp53) or with neo vector (SAS/neo) were injected subcutaneously into hind legs of nude mice. Tumor-bearing mice received 5-bromo-2’-deoxyuridine (BrdU) continuously to label all intratumor proliferating (P) cells. They received γ-rays or accelerated carbon-ion beams at a high or reduced dose-rate. Other tumor-bearing mice received reactor thermal or epithermal neutrons at a reduced dose-rate. Immediately or 9 hours after the high dose-rate irradiation (HDRI), or immediately after the reduced dose-rate irradiation (RDRI), the tumor cells were isolated and incubated with a cytokinesis blocker, and the micronucleus (MN) frequency in cells without BrdU labeling (Q cells) was determined using immunofluorescence staining for BrdU. Results: The difference in radiosensitivity between the total (P + Q) and Q cells after γ-ray irradiation was markedly reduced with reactor neutron beams or carbon-ion beams, especially with a higher linear energy transfer (LET) value. Following γ-ray irradiation, SAS/neo tumor cells, especially intratumor Q cells, showed a marked reduction in sensitivity due to the recovery from radiation-induced damage, compared with the total or Q cells within SAS/mp53 tumors that showed little repair capacity. In both total and Q cells within both SAS/neo and SAS/mp53 tumors, carbon-ion beam irradiation, especially with a higher LET, showed little recovery capacity through leaving an interval between HDRI and the assay or decreasing the dose-rate. The recovery from radiation-induced damage after γ-ray irradiation was a p53-dependent event, but little recovery was found after carbon-ion beam irradiation. With RDRI, the radiosensitivity to reactor thermal and epithermal neutron beams was slightly higher than that to carbon-ion beams. Conclusion: For tumor control, including intratumor Q-cell control, accelerated carbon-ion beams, especially with a higher LET, and reactor thermal and epithermal neutron beams were very useful for suppressing the recovery from radiation-induced damage irrespective of p53 status of tumor cells