Abstract Antibodies to Ro52/tripartite motif-containing 21 (TRIM21), referred to as anti-Ro52, are found in patients diagnosed with diverse systemic autoimmune rheumatic disease and associated with interstitial lung diseases. However, little is known about the clinical characteristics of anti-Ro52 in patients with idiopathic interstitial pneumonias (IIPs). We aimed to analyze the prevalence, co-existent autoantibodies, and clinical characteristics of anti-Ro52 in patients with IIP. The study enrolled 288 patients diagnosed with IIP. Clinical, laboratory and radiographic findings of IIP patients were compared between anti-Ro52 positives and negatives. Anti-Ro52 (20/288; 6.9%), anti-ARS (18/288; 6.3%), and anti-Ro60/SS-A (16/288; 5.6%) were the most common autoantibodies detected in IIP patients. Among 20 IIP patients who had anti-Ro52, anti-ARS was present in 8 (40%) patients. The criteria for interstitial pneumonia with autoimmune features (IPAF) were significantly better fulfilled by patients with anti-Ro52 than those without (P = 0.001). Meeting serological domain (P < 0.001) and Raynaud’s phenomenon (P = 0.009) were significantly more common in the anti-Ro52-positive patients. Anti-Ro52-positive IIP patients have clinical features consistent with IPAF. Anti-Ro52 may have an important role in detecting the autoimmune phenotype in IIP patients.
Background and objective: COPD is a multifactorial disease influenced by genetic and environmental factors, and gene‐by‐environmental interactions. There is considerable variability in the degree of airflow obstruction, moreover only 10–15% of chronic smokers develop COPD. These observations indicate that additional risk factors, possibly genetic, contribute to not only the susceptibility to COPD but also the development and severity of COPD. Recent paradigms highlight the presence and causal role of apoptosis in emphysema. There is a large amount of information on the genes involved in the regulation of apoptosis and one of the most studied is Bcl‐2 . The aim of this study was to investigate the genetic association of Bcl‐2 gene with the level of lung function, that is, the severity, of COPD. Methods: The genetic association of Bcl‐2 polymorphisms with lung function was investigated in 261 Japanese patients with COPD using 12 single‐nucleotide polymorphisms (SNPs) in Bcl‐2 . Results: Four SNPs showed a significant association between the high and low lung function groups in a dominant trait comparison. Subsequent linkage‐disequilibrium mapping and analyses of haplotype structure also showed a significant association between the level of lung function and two haplotypes comprised of the associated SNPs in Bcl‐2 . Conclusions: Although the linkage between Bcl‐2 gene and the susceptibility to COPD remains to be clarified, the findings of the current study indicate that Bcl‐2 might be influencing the level of lung function, that is, the development and severity of COPD.
Multifocal micronodular pneumocyte hyperplasia (MMPH) is pathologically characterized by multifocal nodular hyperplasia of type Ⅱ pneumocyte-like cells. MMPH is usually complicated with tuberous sclerosis complex (TSC). MMPH patients tend to be asymptomatic or only slightly symptomatic. MMPH tends to progress slowly and needs no treatment. We herein describe two cases of MMPH with its characteristic radiological features and clinical manifestations of TSC. Case 1: a 20-year-old female with definitive TSC in infancy. Chest CT at the age of 18 revealed multiple nodular opacities and ground-glass attenuations in a scattered and random distribution in the bilateral lungs. Case 2: a 44-year-old female with probable TSC at 36 years of age. Chest CT at the age of 43 showed random areas of small ground-glass attenuations, predominantly in the upper lung fields. Case 1 and Case 2 have had no respiratory symptoms or radiographic changes in the recent two years and four years, respectively. Although pathological examinations of the lung were not performed because consent for surgical lung biospies was unobtainable, we considered that these pulmonary manifestations were most likely MMPH with TSC because of these characteristic radiographical findings of multiple nodular opacities and ground-glass attenuations of 10 mm or less in size and their scattered distribution, and because there have been no abnormal laboratory data or changes in their chest radiological findings for years. Neither patient is under treatment for pulmonary lesions. Although MMPH is a rare disease, multiple nodules and ground-glass attenuations on lung imaging findings should be considered as pulmonary manifestations in patients with TSC.
Abstract Purpose Many patients with lung cancer have cancer cachexia, which may result in complications and affect prognosis; however, its preoperative prevalence is unknown. Skeletal muscle mass loss after lung cancer surgery also affects prognosis. Although cachexia and sarcopenia share some similarities, whether preoperative cachexia affects postoperative sarcopenia is still unknown. Thus, we designed a cohort study of patients with non-small cell lung cancer (NSCLC) to investigate this. Methods Patients with NSCLC who underwent surgery and perioperative rehabilitation were included in this study. The prevalence of preoperative cachexia and association between preoperative cachexia and sarcopenia 1 month after surgery were tested using propensity-score matching. After matching, the regression analysis was performed to investigate whether preoperative cachexia was independently related to sarcopenia 1 month postoperatively. Results In total, 126 patients (73 men) aged 71 (67, 76) years were included in the study. Preoperative cachexia was present in 16 (12.7%) patients, and postoperative sarcopenia was present in 29 (23%) patients. Among the 126 patients, 16 and 32 patients were included in the preoperative cachexia and control groups, respectively, as a result of matching (standardized mean difference < 0.1). After matching, regression analysis showed that preoperative cachexia was independently associated with sarcopenia at 1 month postoperatively (Odd: 1.46, p = 0.020). Conclusions Among the patients with NSCLC, 12.7% had preoperative cachexia. Preoperative cachexia in patients with NSCLC affected sarcopenia 1 month postoperatively.
To determine whether alveolar epithelial cell (AEC) apoptosis via caspase activation is involved in asbestos-induced lung injury, we examined apoptosis, caspase-3 and-9 activation using chrysotile asbestos exposure models in vitro and in vivo. Apoptotic cells were assessed in A549 cells with terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) method after 48 hours exposure of chrysotile asbestos (5 to 100 ug/cm2). Asbestos exposure induced a dose-dependent increase of apoptotic cells, and both pretreatment with Z-LEHD-FMK (caspase-3 inhibitor) or Z-DEMK-FMK (caspase-9 inhibitor) significantly suppressed asbestos-induced apoptosis. Expression of cleaved caspase-3 and-9 increased significantly from 18 to at least 48 hours after asbestos exposure. In vivo study, either 1 or 2 mg of chrysotile asbestos were administered into rat lungs intratracheally, and the lungs were obtained 3 days, 1 and 2 weeks, 1, 3 and 6 months after the administration. Asbestos exposure increased the number of apoptotic cells and the activation of cleaved caspase-3 and -9 most at 3 days in a dose dependent manner, and continued to increase them until at least 6 months after asbestos exposure. Apoptotic cells and cleaved caspase-3 and -9 positive cells were mainly observed in AECs. These findings suggest that AEC apoptosis via caspase-3 and -9 activation is involved in asbestos-induced lung injury.
The AAAI 2023 spring symposium on “Socially Responsible AI for Well-Being” was held at Hyatt Regency San Francisco Airport, California, from March 27th to 29th. AI has great potential for human well-being but also carries the risk of unintended harm. For our well-being, AI needs to fulfill social responsibilities such as fairness, accountability, transparency, trust, privacy, safety, and security, not just productivity such as exponential growth and economic and financial supremacy. For example, AI diagnostic systems must not only provide reliable results (for example, highly accurate diagnostic results and easy-to-understand explanations) but also their results must be socially acceptable (for example, data for AI [machine learning] must not be biased (the amount of data for training must not be biased by race or location (for example, the amount of data for learning must be equal across races and locations). As in this example, AI decisions affect our well-being, suggesting the importance of discussing “what is socially responsible” in several potential well-being situations in the coming AI era. The first perspective is “(Individual) Responsible AI” and aims to identify what mechanisms and issues should be considered to design responsible AI for well-being. One of the goals of responsible AI for well-being is to provide accountable outcomes for our ever-changing health conditions. Since our environment often drives these changes in health, Responsible AI for Well-Being is expected to offer responsible outcomes by understanding how our digital experiences affect our emotions and quality of life. The second perspective is “Socially Responsible AI,” which aims to identify what mechanisms and issues should be considered to realize the social aspects of responsible AI for well-being. One aspect of social responsibility is fairness, that is, that the results of AI should be equally helpful to all. The problem of “bias” in AI (and humans) needs to be addressed to achieve fairness. Another aspect of social responsibility is the applicability of knowledge among people. For example, health-related knowledge found by an AI for one person (for example, tips for a good night's sleep) may not be helpful to another person, meaning that such knowledge is not socially responsible. To address these problems, we must understand how fair is fair and find ways to ensure that machines do not absorb human bias by providing socially responsible results. Our symposium included 18 technical presentations over 2-and-a-half days. Presentation topics included (1) socially responsible AI, (2) communication and evidence for well-being, (3) face expression and impression for well-being, (4) odor for well-being, (5) ethical AI, (6) robot Interaction for social well-being, (7) communication and sleep for social well-being, (8) well-being studies, (9) information and sleep for social well-being For example, Takashi Kido, Advanced Comprehensive Research Organization of Teikyo University in Japan, presented the challenges of socially responsible AI for well-being. Oliver Bendel, School of Business FHGW in Switzerland, presented the increasing well-being through robotic hugs. Martin D. Aleksandrov, Freie Universitat Berlin in Germany, presented the limiting inequalities in the fair division with additive value preferences for indivisible social items. Melanie Swan, University College London in the United Kingdom, presented Quantum intelligence, responsible human machine entities. Dragutin Petkovic, San Francisco State University in Unites States, presented on San Francisco State University Graduate Certificate in Ethical AI. Our symposium provides participants unique opportunities where researchers with diverse backgrounds can develop new ideas through innovative and constructive discussions. This symposium will present significant interdisciplinary challenges for guiding future advances in the AI community. Takashi Kido and Keiki Takadama served as co-chairs of this symposium. The papers of the symposium will be published online at CEUR-WS.org. The authors declare no conflicts of interest. Takashi Kido is a professor at Teikyo University in Japan. He had been a visiting researcher at Stanford University. Keiki Takadama is a professor at the University of Electro-Communications in Japan.
Understanding the human mind and increasing individual happiness are important goals in artificial intelligence (AI) and well-being science. The recent revolution in portable self-tracking devices in the data-driven wellness movement and participatory-driven wellness communities, such as the Quantified Self community, provides us with new opportunities to collect psychological or physiological data for understanding the human mind. While new technologies make it possible to track our daily behavior and various biological signals such as physiological or genetic data more easily, one of the important remaining challenges is to discover our own truly meaningful personal values. Citizen science, scientific research by crowdsourcing or human-based computation, is a new and challenging framework that promotes interdisciplinary research in the fields of computer science, life/brain science, and social psychological/behavioral science, which may introduce new paradigms to the AI community. We have been working on citizen science projects related to the area of personal genomics and have developed a personal genomics information environment named MyFinder. The developed platform supports the search for our inherited talents and maximizes our potential for a meaningful life. In particular, we are interested in the human mind and the personal genome. In this paper, we introduce our MyFinder Project and present the results of a recent study on “social intelligence genomics and empathy building”, and discuss issues involved in exploring our mind within the context of personal genomics.
Background Molecular biological modalities with better detection rates have been applied to identify the bacteria causing infectious diseases. Approximately 10–48% of bacterial pathogens causing community-acquired pneumonia are not identified using conventional cultivation methods. This study evaluated the bacteriological causes of community-acquired pneumonia using a cultivation-independent clone library analysis of the 16S ribosomal RNA gene of bronchoalveolar lavage specimens, and compared the results with those of conventional cultivation methods. Methods Patients with community-acquired pneumonia were enrolled based on their clinical and radiological findings. Bronchoalveolar lavage specimens were collected from pulmonary pathological lesions using bronchoscopy and evaluated by both a culture-independent molecular method and conventional cultivation methods. For the culture-independent molecular method, approximately 600 base pairs of 16S ribosomal RNA genes were amplified using polymerase chain reaction with universal primers, followed by the construction of clone libraries. The nucleotide sequences of 96 clones randomly chosen for each specimen were determined, and bacterial homology was searched. Conventional cultivation methods, including anaerobic cultures, were also performed using the same specimens. Results In addition to known common pathogens of community-acquired pneumonia [Streptococcus pneumoniae (18.8%), Haemophilus influenzae (18.8%), Mycoplasma pneumoniae (17.2%)], molecular analysis of specimens from 64 patients with community-acquired pneumonia showed relatively higher rates of anaerobes (15.6%) and oral bacteria (15.6%) than previous reports. Conclusion Our findings suggest that anaerobes and oral bacteria are more frequently detected in patients with community-acquired pneumonia than previously believed. It is possible that these bacteria may play more important roles in community-acquired pneumonia.
