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Body talk is how people talk with others about their bodies, classified into three types based on its content: negative fat talk, negative muscle talk, and positive body talk. Negative fat talk is complaining about being fat or losing weight. Negative muscle talk is discussing the desire or the obligation to build muscles. Positive body talk is conversations about accepting or affirming the body and eating habits (Lin et al., 2021). Studies have suggested that negative fat talk is positively associated, whereas positive body talk is negatively associated with body fat dissatisfaction, especially among women (Arroyo et al., 2022; Lin et al., 2021; Takamura et al., 2019). However, previous studies did not indicate the causality between these variables. This longitudinal study plans to investigate the causal relationships between these two types of body talk and body dissatisfaction using a questionnaire to evaluate the participants’ subjective body dissatisfaction and the discrepancy between the ideal and actual body image. The study also plans to examine whether negative fat talk and positive body talk moderate the association between exposure to thin-ideal images on the Internet and body dissatisfaction. Research has suggested that exposure to ideal images, including peers or celebrities, on the Internet, is associated with body dissatisfaction (Rounsefell et al., 2019). Fardouly and Vartanian (2015) suggested that engaging in Facebook photo activities was associated with body dissatisfaction due to comparing own body shape with others. This study will examine whether negative fat talk can increase the association between exposure to thin-ideal images on the Internet and body fat dissatisfaction, whereas positive body talk can decrease this association for reasons described in the Hypotheses section. A previous study of men and women indicated that negative muscle talk is associated with increased maladaptive muscle gain behaviors and dissatisfaction regarding body size and shape (Lin et al., 2021; Sladek et al., 2014), suggesting that people who engage in negative muscle talk have internalized an athletic body shape. However, previous studies have not extensively studied the influence of negative muscle talk. Therefore, the current study plans to use a longitudinal design to examine the effect of negative muscle talk. This study will investigate the longitudinal associations among the variables described above in female university students because the desire to be thin is a problem observed mainly in young Japanese women (Ministry of Health, Labour and Welfare, 2019). However, the current study also explores the effects of the study variables on male students.

It is assumed that the personality traits of interpersonal sensitivity and privileged self are related to the new type of depression (Sakamoto, Muranaka, & Yamakawa, 2014). A previous longitudinal study by Muranaka, Yamakawa, and Sakamoto (2019) indicated that interpersonal sensitivity and privileged self could generate interpersonal stress. However, this study had the limitation that it examined the effects of interpersonal sensitivity and privileged self at baseline on interpersonal stress during the follow-up period without controlling for the influence of interpersonal stress experienced before the baseline. As a result, it is uncertain whether Muranaka et al. demonstrated the effect of interpersonal sensitivity and privileged self on subsequently increased interpersonal stress. In addition, Muranaka et al. did not specifically assess experiences of event categories related to stress generation. Therefore, we designed the present study to examine the stress-generating effect of interpersonal sensitivity and privileged self by improving the limitations of Muranaka et al.

Yoshikazu Yamaguchi,1– 3 Tetsuya Miyashita,1 Yuko Matsuda,1 Makoto Sasaki,1 Shunsuke Takaki,1 Stephani S Kim,2 Joseph D Tobias,2,3 Takahisa Goto1 1Department of Anesthesiology and Critical Care, Yokohama City University, Kanagawa, Japan; 2Department of Anesthesiology and Pain Medicine, Nationwide Children’s Hospital, Columbus, OH, USA; 3Department of Anesthesiology and Pain Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USACorrespondence: Yoshikazu YamaguchiDepartment of Anesthesiology and Pain Medicine, Nationwide Children’s Hospital, Columbus, OH 43205, USATel +1 (614) 722-4200Fax +1 (614) 722-4203Email yoshikaz@rd6.so-net.ne.jpBackground: Precise control of tidal volume is one of the keys in limiting ventilator-induced lung injury and ensuring adequate ventilation in mechanically ventilated neonates. The aim of the study was to compare the tidal volume (mVT) measured from the expiratory limb of the ventilator with the actual tidal volume (aVT) that would be delivered to the patient using a lung model to simulate a neonate.Methods: This study was conducted using the ASL5000 lung simulator. Three combinations of parameters were set: resistance (cmH2O/L/sec) and compliance (mL/cmH2O) of 50 and 2 (Group 1), 100 and 1 (Group 2), and 150 and 0.5 (Group 3), respectively. The ASL5000 was connected to each of the ventilators including one anesthesia machine ventilator (Drager Fabius GS) and two ICU ventilators (Servo-i Universal and Evita Infinity V500). Each ventilator was evaluated with a set tidal volume of 30 mL (sVT) and a respiratory rate of 25 breathes/minute in both the volume-controlled ventilation (VCV) and dual-controlled ventilation (DCV) modes.Results: The discrepancies between sVT, mVT and aVT were highest with the Fabius anesthesia machine ventilator and increased in the simulated lung injury groups. When comparing the ICU ventilators, the difference was greater the Servo-i and increased when using the DCV mode and with simulated lung injury.Conclusion: Accurate tidal volumes were achieved only with the Infinity ICU ventilator. This was true regardless of mode of ventilation and even during simulated lung injury.Keywords: mechanical ventilation, pediatric anesthesia, tidal volume, flow sensor, lung protective ventilation, volutrauma

SUMMARY: Amelogenin is one of the enamel matrices secreted by ameloblasts. A mutation of the amelogenin gene can cause hereditary dental enamel defects known as amelogenesis imperfecta (AI). Since lysosome-associated membrane protein-1 (LAMP-1), -3 (LAMP-3), and 78kDa glucose-related protein (Grp78) were identified as binding proteins of amelogenin, several studies have suggested the involvement of these binding proteins with the cell kinetics of ameloblasts in normal or abnormal conditions. The purpose of this study is to investigate the distribution of these amelogenin binding proteins in the ameloblast cell differentiation of mice with a point mutation of the amelogenin gene (Amelx*). The incisors of Amelx* mice had a white opaque color and the tooth surface was observed to be rough under a scanning electron microscope. Among the sequential ameloblast cell differentiation in the Amelx* mice, the shape of ameloblasts at the transition stage was irregular in comparison to those in wild-type (WT) mice. Immunostaining of Grp78 revealed that the whole cytoplasm of the transition stage ameloblasts was immunopositive for Grp78 antibody, while only the distal part of cell was positive in the WT mice. Furthermore, in the Amelx* mice, the cytoplasm of the transition stage ameloblasts was immunopositive for LAMP-1 and LAMP-3. These results suggest that Amelx* may cause the abnormal distribution of amelogenin binding proteins in the cytoplasm of ameloblasts. RESUMEN: La amelogenina es una de las matrices de esmalte secretadas por los ameloblastos. Una mutación del gen de amelogenina puede causar defectos hereditarios del esmalte dental conocidos como amelogénesis imperfecta (AI). Dado que la proteína de membrana asociada a lisosoma-1 (LAMP-1), -3 (LAMP-3) y la proteína relacionada con la glucosa de 78 kDa (Grp78) se identificaron como proteína de unión a amelogenina, varios estudios han sugerido la participación de estas proteínas con la cinética celular de los ameloblastos en condiciones normales o anormales. El objetivo del estudio fue investigar la distribución de LAMP-1, LAM-3 y Grp78 durante la diferenciación celular de ameloblastos de ratones con una mutación puntual del gen de amelogenina (Amelx*). Los incisivos de los ratones Amelx* presentaron un color blanco opaco y se observó en microscopio electrónico de barrido que la superficie del diente era áspera. La diferenciación celular secuencial y la forma de los ameloblastos en la etapa de transición en los ratones Amelx* fue irregular en comparación con los ratones silvestres (RS). La inmunotinción de Grp78 reveló que todo el citoplasma de los ameloblastos en etapa de transición fue inmunopositivo para el anticuerpo Grp78, mientras que solo la parte distal de la célula fue positiva en los ratones RS. Además, en ratones Amelx*, el citoplasma de los ameloblastos en etapa de transición fue inmunopositivo para LAMP-1 y LAMP-3. Estos resultados sugieren que Amelx* puede causar distribución anormal de proteínas de unión a amelogenina en el citoplasma de los ameloblastos.