Corrigendum to "Cigarette smoke, but not novel tobacco vapor products, causes epigenetic disruption and cell apoptosis" [Biochem. Biophys. Rep. 24 (2020) 100865].

[This corrects the article DOI: 10.1016/j.bbrep.2020.100865.].

Compounds in cigarette smoke induce EGR1 expression via the AHR, resulting in apoptosis and COPD.

Chronic obstructive pulmonary disease (COPD) is a major cause of mortality worldwide, and pulmonary epithelial cell apoptosis is regarded as one of the most important factors in its pathogenesis. Here, we examined the molecular mechanisms of apoptosis caused by cigarette smoke (CS). In the normal bronchial epithelium cell line BEAS-2B, a CS extract markedly induced apoptosis together with transient early growth response 1 (EGR1) protein expression, which is activated over time via the aryl hydrocarbon receptor (AHR). The CS extract-induced apoptosis decreased cell count of BEAS-2B cells and was significantly reversed by knockdown of either EGR1 or AHR. In vivo, the CS extract caused alveolar wall destruction, mimicking COPD, 1 week after intrathoracic injection. Bronchoalveolar lavage fluid (BALF) from the CS extract-treated mice contained massive numbers of apoptotic epithelial cells. Furthermore, it was found that aminoanthracene induced EGR1 expression and cell apoptosis. By contrast, the AHR antagonist stemregenin 1 (SR1) restored apoptosis upon CS treatment. These results suggest that aryl hydrocarbons, such as aminoanthracene, induce EGR1 expression via the AHR, resulting in cell apoptosis and that this can be prevented by administration of an antagonist of AHR.

Cigarette smoke, but not novel tobacco vapor products, causes epigenetic disruption and cell apoptosis.

Heat-Not-Burn (HNB) products, generating vapor without combusting tobacco leaves, have been developed with the expectation that the number and quantity of chemicals in the vapor of these products would be reduced compared with the smoke from conventional combustible cigarettes. However, whether the lower chemical levels correlate with lower toxicity remains to be determined. Here we examined differences in the biological effects of conventional cigarette smoke (CS) and two HNB products, Ploom TECH and Ploom TECH+, using the cultured cancer cell line A549 and the normal bronchial epithelium cell line BEAS-2B. The conventional CS 3R4F extract (0.5%) markedly decreased cell proliferation of both A549 and BEAS-2B cells; however, 0.5% extracts of these commercially available HNB products did not affect cell growth. To determine the cause of decreased cell proliferation, a TUNEL assay was performed, and the results indicated that apoptosis had occurred in both A549 and BEAS-2B cells at 24 h after exposure to 3R4F. To further explore the effect of CS on epigenetics, we performed western blotting to detect histone H2A phosphorylation, which is known to affect transcriptional regulation. Only the 3R4F extract decreased histone H2A phosphorylation in both A549 and BEAS-2B cells. Next, we examined alterations in gene expression after treatment of A549 cells with Ploom TECH, Ploom TECH+, or 3R4F extracts. It was found that 339, 107, and 103 genes were upregulated more than 2 fold in A549 cells treated with 3R4F, Ploom TECH, or Ploom TECH + extracts, respectively. Among the 339 genes that were upregulated in response to 3R4F, we focused on EGR1, FOS, and FOSB, since they were upregulated more than 100 fold, which was confirmed using RT-qPCR. These results suggest that CS, but not HNB products, cause epigenetic disruption and cell apoptosis, possibly by elevating transcription of genes such as EGR1.

Comparison of the predictability of neurological outcome by serum procalcitonin and glial fibrillary acidic protein in postcardiac-arrest patients.

BACKGROUND: In past research, procalcitonin (PCT) and glial fibrillary acidic protein (GFAP) have been reported to be useful biomarkers in predicting neurological outcome after the return of spontaneous circulation (ROSC) following out-of-hospital cardiac arrest (CA), although they have only been studied separately. In this study, we compared the usefulness of PCT and GFAP in predicting neurological outcome. METHODS: This study was a retrospective, single-center analysis, conducted in the intensive-care unit of a university hospital. Twenty-one sequential post-CA patients were included. Serum samples were collected from patients at 12 and 24 h after ROSC. Serum PCT and GFAP were measured and compared in patients with favorable and unfavorable neurological outcomes, evaluated at 6 months using the Glasgow-Pittsburgh Cerebral Performance Categories. RESULTS: Serum PCT was significantly higher at 12 and 24 h in patients with unfavorable outcomes (P = 0.004 and 0.002, respectively). Serum GFAP was not significantly higher at 12 and 24 h in patients with unfavorable outcomes (P = 0.118 and 0.079, respectively). The combination of PCT and GFAP showed high predictive value for unfavorable outcomes (86.7% sensitivity and 100% specificity at 12 h; 100% sensitivity and 83.3% specificity at 24 h). CONCLUSION: Serum PCT is a marker of unfavorable neurological outcome in post-CA patients, and is superior to serum GFAP in the early phase.

[Acute poisoning with neonicotinoid insecticide acetamiprid].

Acetamiprid belongs to a new class of insecticides called neonicotinoids, which have different effects from other insecticides. Neonicotinoids act as selective agonists at the nicotinic acetylcholine receptors, therefore their toxicity is higher to insect pests than to humans. Cases of acetamiprid poisoning are still rare, because neonicotinoids have been released in the market only within the last decade. We experienced a case of acute acetamiprid poisoning and measured the blood concentration of acetamiprid. A 79-year-old man had ingested acetamiprid and got medical attention two hours after ingestion. On arrival, he had consciousness disturbance (GCS-8), hypotension, nausea, vomiting and hyperglycemia, but had no constricted pupils nor mucous supersecretion which are characteristic in organophosphate poisoning. Gastric lavage was performed and activated charcoal and laxative were administered. Paroxysmal atrial fibrillation persisted until 11 hours after ingestion. The next day, his symptoms with regards to the effects of acetamiprid improved and he was discharged from the hospital without complication. Blood concentration of acetamiprid on arrival, approximately 2 hours after the ingestion, was 21.1 microg/ml.