Hedonic Risk Preference Associated with High-Risk Behaviors under COVID-19 Pandemic among Medical Students in Japan.

BACKGROUND: Public health measures to mitigate the spread of COVID-19 have focused on raising awareness and disseminating knowledge. Few considered people's risk preferences and no measurement was adapted to the context of COVID-19. This study aims (1) to investigate the association between risk preference and risk behaviors and (2) to compare a novel hedonic preference question with traditional risk preference assessment tools in the context of the COVID-19 pandemic among medical students in Japan. METHODS: An online survey of fourth-year medical students was conducted. Logistic regression analysis adjusted for gender, age, household income, and the overconfidence effect were performed to investigate the association. RESULTS: We observed significantly higher odds of high-risk behaviors in general risk preference (odds ratio (OR): 4.04; 95% confidence interval (CI): 1.05-15.50) and hedonic preference (OR: 6.58; 95% CI: 1.86-23.28) when adjusted, whereas monetary preference showed no significant association. Concerning specific risky behaviors, hedonic preference were significantly associated with four items after adjusting for covariates ("dine out" (OR: 2.78, 95% CI: 1.13-6.85), "go out" (OR: 4.35, 95% CI: 1.65-11.46), "not practicing safety precautions" (OR: 2.79, 95% CI: 1.11-7.04) and "travel" (OR: 4.36, 95% CI: 1.42-13.44)), and general preference in two ("dine out" (OR: 4.82, 95% CI: 1.66-14.00) and "go out" (OR: 6.48, 95% CI: 2.07-20.24)). CONCLUSION: Hedonic and general risk preferences were significantly associated with high-risk behaviors during the COVID-19 pandemic. Future application of the novel risk-for-pleasure-seeking preference question is warranted.

Association between Cooperative Attitude and High-Risk Behaviors on the Spread of COVID-19 Infection among Medical Students in Japan.

The impact of high-risk behaviors on the spread of COVID-19 infection among young people is an important problem to address. This study analyzed the association between cooperativeness and high-risk behaviors. We conducted a cross-sectional study among fourth-year medical students at Tokyo Medical and Dental University. The students were asked about cooperative attitude in a hypothetical situation of performing a task together with an unfamiliar classmate, who did not cooperate to complete the task previously. The response items were as follows: "cooperate", "don't want to cooperate and do it alone (non-cooperative)", and "don't want to cooperate and let the partner do it alone (punishment)". Eating out and vaccine hesitancy were also treated as high-risk behaviors. Poisson regression was used to investigate the association between cooperative attitude and each high-risk behavior, adjusted for demographics. Of the 98 students, 23 (23.5%), 44 (44.9%), and 31 (31.6%) students chose "noncooperative", "cooperative", and "punishment", respectively. Cooperative-type students exhibited 2.77-fold (PR: 2.77, 95% CI: 1.03-7.46), and punishment-type students exhibited 3.16-fold greater risk of eating or drinking out (PR: 3.16, 95% CI: 1.14-8.75) compared with those of the noncooperative type. Among medical students, the "cooperative" type and "punishment" type comprised the high-risk group for eating out during the pandemic.

Structural basis for the oligomerization-mediated regulation of NLRP3 inflammasome activation.

SignificanceThe nucleotide-binding oligomerization domain (NOD)-like receptor pyrin domain containing 3 (NLRP3) is a pattern recognition receptor that forms an inflammasome. The cryo-electron microscopy structure of the dodecameric form of full-length NLRP3 bound to the clinically relevant NLRP3-specific inhibitor MCC950 has established the structural basis for the oligomerization-mediated regulation of NLRP3 inflammasome activation and the mechanism of action of the NLRP3 specific inhibitor. The inactive NLRP3 oligomer represents the NLRP3 resting state, capable of binding to membranes and is likely disrupted for its activation. Visualization of the inhibitor binding mode will enable optimization of the activity of NLRP3 inflammasome inhibitor drugs.

Cardiac arrest during hemodialysis: a survey of five Japanese hospitals.

AIM: Intraprocedural cardiac arrest is a serious complication among patients receiving hemodialysis. However, the frequency and reaction to these events remain unclear. This study aimed to explore the clinical picture of cardiac arrest during hemodialysis. METHODS: Ten cardiac arrests that had occurred during 217,984 hemodialysis treatments in five Japanese hospitals, between 2008 and 2017, were reviewed. We investigated the underlying disease, vital signs, emergency responses, and outcomes using patient medical records. RESULTS: The cardiac arrest rate ranged from 1.1 to 7.5 per 100,000 hemodialysis sessions. All included cases of cardiac arrest occurred in a hemodialysis unit and had been witnessed and reported by supervising clinicians. The initial rhythm was ventricular fibrillation/ventricular tachycardia in six patients (60%) and pulseless electrical activity/asystole in four patients (40%). Seven (70%) patients showed a return of spontaneous circulation (ROSC), and two (20%) patients were discharged with a cerebral performance category score of 1. There was a statistically significant difference in the ROSC rate (P = 0.048) only in the event of an emergency call. The SpO2 and respiratory rates had not been recorded in six patients. There was no significant difference in ROSC between initial rhythms of ventricular fibrillation/ventricular tachycardia and pulseless electrical activity/asystole. CONCLUSION: We evaluated the frequency of cardiac arrest during hemodialysis. Overall assessment including respiratory status is needed at initiation of hemodialysis. In case of a sudden change in a patient's status, high-quality resuscitation treatment that includes an emergency call can improve prognosis.

An attenuated LC16m8 smallpox vaccine: analysis of full-genome sequence and induction of immune protection.

The potential threat of smallpox bioterrorism has made urgent the development of lower-virulence vaccinia virus vaccines. An attenuated LC16m8 (m8) vaccine was developed in 1975 from the Lister strain used in the World Health Organization smallpox eradication program but was not used against endemic smallpox. Today, no vaccines can be tested with variola virus for efficacy in humans, and the mechanisms of immune protection against the major intracellular mature virion (IMV) and minor extracellular enveloped virion (EEV) populations of poxviruses are poorly understood. Here, we determined the full-genome sequences of the m8, parental LC16mO (mO), and grandparental Lister (LO) strains and analyzed their evolutionary relationships. Sequence data and PCR analysis indicated that m8 was a progeny of LO and that m8 preserved almost all of the open reading frames of vaccinia virus except for the disrupted EEV envelope gene B5R. In accordance with this genomic background, m8 induced 100% protection against a highly pathogenic vaccinia WR virus in mice by a single vaccination, despite the lack of anti-B5R and anti-EEV antibodies. The immunogenicity and priming efficacy with the m8 vaccine consisting mainly of IMV were as high as those with the intact-EEV parental mO and grandparental LO vaccines. Thus, mice vaccinated with 10(7) PFU of m8 produced low levels of anti-B5R antibodies after WR challenge, probably because of quick clearance of B5R-expressing WR EEV by strong immunity induced by the vaccination. These results suggest that priming with m8 IMV provides efficient protection despite undetectable levels of immunity against EEV.

Mutations and deletions of the CBP gene in human lung cancer.

PURPOSE: Microarray-based comparative genomic hybridization analysis led us to detect a homozygous deletion at the cyclic AMP response element binding protein-binding protein (CBP) locus in a lung cancer cell line. Oncogenic roles of CBP had been suggested by functional and genetic studies; thus, involvement of CBP gene alterations in lung carcinogenesis was investigated by undertaking comprehensive analysis of genetic CBP alterations in human lung cancer. EXPERIMENTAL DESIGN: Fifty-nine cell lines and 95 surgical specimens of lung cancer were analyzed for mutations, homozygous and hemizygous deletions, and expression of the CBP gene. RESULTS: Homozygous CBP deletions, including two intragenic deletions, were detected in three (5.1%) lung cancer cell lines. CBP mutations, including missense, nonsense, and frame-shift mutations, were detected in six (10.2 %) cell lines and five (5.3%) surgical specimens of lung cancer. The wild-type CBP allele was retained in 9 of 11 cases with CBP mutations, and both the wild-type and mutant alleles were expressed in all the six cases with heterozygous CBP mutations examined. Three mutations with amino acid substitutions in the histone acetyltransferase domain caused significant reduction in transcription activation activity of CBP protein in vivo. CONCLUSIONS: A fraction of lung cancers carried mutations and/or deletions of the CBP gene, suggesting that genetic CBP alterations are involved in the genesis and/or progression of a subset of lung cancers.

Association of amino acid substitution polymorphisms in DNA repair genes TP53, POLI, REV1 and LIG4 with lung cancer risk.

Single nucleotide polymorphisms (SNPs) were searched for in 36 genes involved in diverse DNA repair pathways, and 50 nonsynonymous (associated with amino acid changes) SNPs identified were assessed for associations with lung cancer risk by a case-control study consisting of 752 adenocarcinoma cases, 250 squamous cell carcinoma cases and 685 controls. An SNP, Arg72Pro, of the TP53 gene encoding a DNA damage response protein showed the strongest association with squamous cell carcinoma risk (OR Pro/Pro vs. Arg/Arg = 2.2), while 2 other SNPs, Phe257Ser of the REV gene encoding a translesion DNA polymerase and Ile658Val of the LIG4 gene encoding a DNA double-strand break repair protein, also showed associations (OR Ser/Ser vs. Phe/Phe = 2.0 and OR Ile/Val vs. Ile/Ile = 0.4, respectively). An SNP, Thr706Ala, in the POLI gene encoding another translesion DNA polymerase was associated with adenocarcinoma and squamous cell carcinoma risk, particularly in individuals of ages < 61 years (OR Ala/Ala + Ala/Thr vs. Thr/Thr = 1.5 and 2.4, respectively). POLI is the human counterpart of PolI, a strong candidate for the Par2 (pulmonary adenoma resistance 2) gene responsible for adenoma/adenocarcinoma susceptibility in mice. The present results suggest that these 4 SNPs function as genetic factors underlying lung cancer susceptibility by modulating activities to maintain the genome integrity of each individual.