Objectives: Neutrophil/lymphocyte ratio (NLR), monocyte/lymphocyte ratio (MLR), and platelet/lymphocyte ratio (PLR) are inflammatory biomarkers. Potential of these inflammatory biomarkers as state marker of schizophrenia severity is controversial. This study aimed to investigate the relationship between inflammatory biomarkers and schizophrenia severity. Methods: From January 2010 to June 2020, the medical records of schizophrenia patients admitted to Kosin University Gospel Hospital were retrospectively examined and 91 patients who met the inclusion criteria were selected as the subjects of the study. The Korean version of the Positive and Negative Syndrome Scale (PANSS-KV) was used to assess schizophrenia symptom severity and divided into PANSS-KV total score (PANSS-T), PANSS-KV positive syndrome subscale (PANSS-P), PANSS-KV negative syndrome subscale (PANSS-N), PANSS-KV general psychopathology subscale (PANSS-G). Results: In 91 subjects, 40 were male and 51 were female. We found no significant relationship between sex, age, number of hospitalization and NLR, MLR, PLR. Patients with higher NLR, MLR, PLR had higher PANSS-T scores. Positive correlation between NLR, MLR, PLR and PANSS-N, PANSS-G was demonstrated. There was no significant correlation between NLR, MLR, PLR and PANSS-P. Conclusions We investigate the possibility of inflammatory biomarkers as state markers of schizophrenia symptom severity. A well-designed prospective study involving a larger cohort is needed in the future.

Sirtuins (SIRTs) are involved in multiple cellular processes. And they are involved in cellular pathways related aging, cancer, and a variety of cellular functions including cell cycle, DNA repair and proliferation. Also they modulate life span. Stem cells have the ability to self-renew for unlimited proliferation and differentiate into various cell types. It has been a little known that the mutation of undifferentiated stem cells in tissue may result in the development of cancer cells by genotoxic carcinogens. Therefore, this study investigated whether some carcinogenic compounds can modulate the expression of sirtuin mRNA on human adipose-derived stem cells. Adipose-derived stem cells (ADSC) were exposed to genotoxic carcinogenic compound (2-nitrofluorene, 2NF) and non-genotoxic carcinogenic compound (clonidine, CND) for 24 hours, 48 hours, 72 hours and 96 hours. The expression of SIRT1 mRNA increased on 72 hours. Expressions of SIRT2 and SIRT7 mRNA increased robustly on 48 hours. But all of SIRTs decreased to a level before a treatment of genotoxic compound on adipose-derived stem cells. These results demonstrated that a treatment of genotoxic compound induced the expression of SIRT mRNA only in the short time. But their level returned to untreated cells on 96 hours. They suggest that the possibility that the sirtuins can retard the carcinogenesis of adipose derived stem cells.
Aging ; Carcinogenesis ; Carcinogens ; Cell Cycle ; Clonidine* ; DNA Repair ; Humans ; RNA, Messenger* ; Sirtuins ; Stem Cells*

Fibromyalgia is a disorder characterized by the core symptom of chronic widespread pain, along with fa-tigue, sleep disturbances, mood changes, and cognitive difficulties. The etiology of fibromyalgia involves a combination of biological factors, such as genetic vulnerability, alterations in pain processing and stress response system ; psychological factors, such as anxiety, depression, anger, and perceived stress ; environmentalfactors, such as infections, febrile diseases, and trauma. Central sensitization, which is amplified in the process of sensory stimulation, has been emphasized as a key etiological factor, as supported by enhanced wind-up, delayed aftersensation, decreased nociceptive flexion reflex threshold and functional imaging studies. Several guidelines recommend that a multimodal approach be used to treat fibromyalgia, including both pharmacologicaland non-pharmacological treatments, tailored to each individual, and that clinicians should provide an intellectual framework through sufficient education and emphasis on the importance of self-management. The prevalence of mood disorders, anxiety disorders, and other psychiatric problems is 7-9 times higher in patients with fibromyal-gia than in the general population ; moreover, the association between fibromyalgia and certain psychopatholo-gies or sleep problems has also been suggested. Since psychiatric problems, with shared vulnerabilities and risk factors, interact with fibromyalgia bidirectionally and also affect the disease course, an integrated management approach is needed to determine the risk of comorbidities.

Fibromyalgia is a disorder characterized by the core symptom of chronic widespread pain, along with fa-tigue, sleep disturbances, mood changes, and cognitive difficulties. The etiology of fibromyalgia involves a combination of biological factors, such as genetic vulnerability, alterations in pain processing and stress response system ; psychological factors, such as anxiety, depression, anger, and perceived stress ; environmentalfactors, such as infections, febrile diseases, and trauma. Central sensitization, which is amplified in the process of sensory stimulation, has been emphasized as a key etiological factor, as supported by enhanced wind-up, delayed aftersensation, decreased nociceptive flexion reflex threshold and functional imaging studies. Several guidelines recommend that a multimodal approach be used to treat fibromyalgia, including both pharmacologicaland non-pharmacological treatments, tailored to each individual, and that clinicians should provide an intellectual framework through sufficient education and emphasis on the importance of self-management. The prevalence of mood disorders, anxiety disorders, and other psychiatric problems is 7-9 times higher in patients with fibromyal-gia than in the general population ; moreover, the association between fibromyalgia and certain psychopatholo-gies or sleep problems has also been suggested. Since psychiatric problems, with shared vulnerabilities and risk factors, interact with fibromyalgia bidirectionally and also affect the disease course, an integrated management approach is needed to determine the risk of comorbidities.

Background/Aims: Recent research has increasingly focused on the role of the gastric microbiome in the development of gastric cancer. We aimed to investigate the changes in the microbiome during gastric carcinogenesis in structural and functional aspects, with a specific focus on the association between oral and gastric microbiomes. Methods: We collected saliva, gastric juice, and gastric tissue samples from 141 patients at different stages of gastric carcinogenesis and processed them for microbiome analysis using 16S rRNA gene profiling. The alpha and beta diversities were analyzed, and the differences in microbiome composition and function profiles were analyzed among the groups, as well as the correlation between changes in the oral and gastric microbiomes during carcinogenesis. Results: We observed significant differences in microbial diversity and composition between the disease and control groups, primarily in the gastric juice. Specific bacterial strains, including Schaalia odontolytica, Streptococcus cristatus, and Peptostreptococcus stomatis, showed a significant increase in abundance in the gastric juice in the low-grade dysplasia and gastric cancer groups. Notably, the correlation between the oral and gastric microbiota compositions, increased as the disease progressed. Predictive analysis of the metagenomic functional profiles revealed changes in functional pathways that may be associated with carcinogenesis (ABC transport and two-component systems). Conclusions During gastric carcinogenesis, the abundance of oral commensals associated with cancer increased in the stomach. The similarity in microbial composition between the stomach and oral cavity also increased, implying a potential role of oral-gastric bacterial interactions in gastric cancer development.

Purpose: Recently, there has been a rise in the interest to understand the composition of indoor dust due to its association with lung diseases such as asthma, chronic obstructive pulmonary disease (COPD) and lung cancer. Furthermore, it has been found that bacterial extracellular vesicles (EVs) within indoor dust particles can induce pulmonary inflammation, suggesting that these might play a role in lung disease. Methods: We performed microbiome analysis of indoor dust EVs isolated from mattresses in apartments and hospitals. We developed diagnostic models based on the bacterial EVs antibodies detected in serum samples via enzyme-linked immunosorbent assay (ELISA) in this analysis. Results: Proteobacteria was the most abundant bacterial EV taxa observed at the phylum level while Pseudomonas, Enterobacteriaceae (f) and Acinetobacter were the most prominent organisms at the genus level, followed by Staphylococcus. Based on the microbiome analysis, serum anti-bacterial EV immunoglobulin G (IgG), IgG1 and IgG4 were analyzed using ELISA with EV antibodies that targeted Staphylococcus aureus, Acinetobacter baumannii, Enterobacter cloacae and Pseudomonas aeruginosa. The levels of anti-bacterial EV antibodies were found to be significantly higher in patients with asthma, COPD and lung cancer compared to the healthy control group. We then developed a diagnostic model through logistic regression of antibodies that showed significant differences between groups with smoking history as a covariate. Four different variable selection methods were compared to construct an optimal diagnostic model with area under the curves ranging from 0.72 to 0.81. Conclusions The results of this study suggest that ELISA-based analysis of anti-bacterial EV antibodies titers can be used as a diagnostic tool for lung disease. The present findings provide insights into the pathogenesis of lung disease as well as a foundation for developing a novel diagnostic methodology that synergizes microbial EV metagenomics and immune assays.

Purpose: Recently, there has been a rise in the interest to understand the composition of indoor dust due to its association with lung diseases such as asthma, chronic obstructive pulmonary disease (COPD) and lung cancer. Furthermore, it has been found that bacterial extracellular vesicles (EVs) within indoor dust particles can induce pulmonary inflammation, suggesting that these might play a role in lung disease. Methods: We performed microbiome analysis of indoor dust EVs isolated from mattresses in apartments and hospitals. We developed diagnostic models based on the bacterial EVs antibodies detected in serum samples via enzyme-linked immunosorbent assay (ELISA) in this analysis. Results: Proteobacteria was the most abundant bacterial EV taxa observed at the phylum level while Pseudomonas, Enterobacteriaceae (f) and Acinetobacter were the most prominent organisms at the genus level, followed by Staphylococcus. Based on the microbiome analysis, serum anti-bacterial EV immunoglobulin G (IgG), IgG1 and IgG4 were analyzed using ELISA with EV antibodies that targeted Staphylococcus aureus, Acinetobacter baumannii, Enterobacter cloacae and Pseudomonas aeruginosa. The levels of anti-bacterial EV antibodies were found to be significantly higher in patients with asthma, COPD and lung cancer compared to the healthy control group. We then developed a diagnostic model through logistic regression of antibodies that showed significant differences between groups with smoking history as a covariate. Four different variable selection methods were compared to construct an optimal diagnostic model with area under the curves ranging from 0.72 to 0.81. Conclusions The results of this study suggest that ELISA-based analysis of anti-bacterial EV antibodies titers can be used as a diagnostic tool for lung disease. The present findings provide insights into the pathogenesis of lung disease as well as a foundation for developing a novel diagnostic methodology that synergizes microbial EV metagenomics and immune assays.