Comparison of Optical Properties and Fracture Loads of Multilayer Monolithic Zirconia Crowns with Different Yttria Levels.

Multilayer monolithic zirconia, which incorporates polychromatic layers that mimic natural tooth gradients, offers enhanced aesthetics and functionality while reducing debonding risks and improving fabrication efficiency. However, uncertainties remain regarding the fracture characteristics of multilayer monolithic zirconia crowns under occlusal loading, whether composed of uniform or combined yttria levels. The current study investigated how variations in yttria levels and thicknesses affected the optical properties and fracture loads of multilayer monolithic zirconia. Samples of multilayer monolithic zirconia in the Vita A1 shade were used, while employing 3Y (SZ) and 4Y + 5Y (AZ) yttria levels. The optical properties, including the color difference (ΔEWS) and translucency parameters (TP00), were measured using a digital colorimeter. The fracture loads were analyzed using a universal testing machine, and fractured surfaces were examined under a stereomicroscope. Statistical analyses assessed the impacts of the yttria levels and sample thicknesses on the optical properties. The ΔEWS values of SZ ranged 3.6 to 4.0, while for AZ, ΔEWS at 0.5 mm was 3.9 and <2.6 for other thicknesses. The TP00 values decreased with an increased thickness, with AZ generally exhibiting greater translucency than SZ. In the fracture load investigations, SZ (>1600 N) generally exceeded AZ (>1260 N), with fracture loads notably increasing with thickness, particularly for premolars (SZ > 3270 N, AZ > 2257 N). SZ predominantly exhibited partial and complete fractures, whereas AZ showed fewer non-fracture categorizations. Complete fractures began with dense, irregular cracks that extended outward to reveal smooth surfaces, while premolars subjected to higher loads exhibited concentric ripple-like structures. Partial fractures revealed radial textures indicative of areas of stress concentration. In summary, higher yttria levels were correlated with increased translucency, while variations in the fracture loads primarily stemmed from differences in the tooth position or thickness. Overall, multilayer monolithic zirconia incorporating combined yttria levels of 4Y + 5Y (AZ) offered high translucency, precise color matching, and substantial fracture resistance, rendering it highly suitable for aesthetic and functional dental applications.

Focus on seed cells: stem cells in 3D bioprinting of corneal grafts.

Corneal opacity is one of the leading causes of severe vision impairment. Corneal transplantation is the dominant therapy for irreversible corneal blindness. However, there is a worldwide shortage of donor grafts and consequently an urgent demand for alternatives. Three-dimensional (3D) bioprinting is an innovative additive manufacturing technology for high-resolution distribution of bioink to construct human tissues. The technology has shown great promise in the field of bone, cartilage and skin tissue construction. 3D bioprinting allows precise structural construction and functional cell printing, which makes it possible to print personalized full-thickness or lamellar corneal layers. Seed cells play an important role in producing corneal biological functions. And stem cells are potential seed cells for corneal tissue construction. In this review, the basic anatomy and physiology of the natural human cornea and the grafts for keratoplasties are introduced. Then, the applications of 3D bioprinting techniques and bioinks for corneal tissue construction and their interaction with seed cells are reviewed, and both the application and promising future of stem cells in corneal tissue engineering is discussed. Finally, the development trends requirements and challenges of using stem cells as seed cells in corneal graft construction are summarized, and future development directions are suggested.

Optimizing intubation technique using a single-use video laryngoscope: A comparative study in a simulation model.

Tracheal intubation poses a high risk of infection to medical staff due to Coronavirus disease 2019 (COVID-19) highly infectious nature. To mitigate this risk, various medical devices, including video laryngoscopy, have been developed to assist intubation. This study compared conventional laryngoscopy (Macintosh) and disposable video laryngoscopes (Medcaptain VS-10s and Honestmc Laryngoscope_LA10000) in terms of their use and operation processes. We designed a questionnaire to assess the operator perception of performing intubation with the devices, and statistical analysis was performed on 50 clinical staff members from 2 hospitals who had performed intubation or had learned intubation techniques. The primary outcomes were time to glottic visualization, intubation time, intubation success rate, distance between the operator and training model, and time from glottic visualization to tube insertion. The secondary outcomes were as follows: overall laryngoscope quality, operative feel, maneuverability, ease of use, and video quality. This study showed that video laryngoscopes were superior to conventional laryngoscopes in terms of quality, operative feel, and ease of use. When LA10000 was employed, the intubation success rate was higher, and the operator risk of infection was lower because of the greater distance from the training model. However, the use of video laryngoscopes requires appropriate education and training use of the devices. This study also demonstrated that when participants viewed a simple operation video prior to using video laryngoscopes, tube insertion time was shorter. Overall, video laryngoscopy can provide a safer and more convenient option for clinical medical personnel during pandemics.

The Epidemiology, Management and Therapeutic Outcomes of Subdural Empyema in Neonates with Acute Bacterial Meningitis.

Background: Subdural empyema is one of the more serious complications of bacterial meningitis and therapeutic challenges to clinicians. We aimed to evaluate the clinical characteristics, treatment, and outcome of subdural empyema in neonates with bacterial meningitis. Methods: A retrospective cohort study was conducted in two medical centers in Taiwan that enrolled all cases of neonates with subdural empyema after bacterial meningitis between 2003 and 2020. Results: Subdural empyema was diagnosed in 27 of 153 (17.6%) neonates with acute bacterial meningitis compared with cases of meningitis without subdural empyema. The demographics and pathogen distributions were comparable between the study group and the controls, but neonates with subdural empyema were significantly more likely to have clinical manifestations of fever (85.2%) and seizure (81.5%) (both p values < 0.05). The cerebrospinal fluid results of neonates with subdural empyema showed significantly higher white blood cell counts, lower glucose levels and higher protein levels (p = 0.011, 0.003 and 0.006, respectively). Neonates with subdural empyema had a significantly higher rate of neurological complications, especially subdural effusions and periventricular leukomalacia. Although the final mortality rate was not increased in neonates with subdural empyema when compared with the controls, they were often treated much longer and had a high rate of long-term neurological sequelae. Conclusions: Subdural empyema is not uncommon in neonates with acute bacterial meningitis and was associated with a high risk of neurological complications, although it does not significantly increase the final mortality rate. Close monitoring of the occurrence of subdural empyema is required, and appropriate long-term antibiotic treatment after surgical intervention may lead to optimized outcomes.

Promotion of ROS-mediated apoptosis, G2/M arrest, and autophagy by naringenin in non-small cell lung cancer.

Background: As lung cancer is the leading cause of cancer death worldwide, the development of new medicines is a crucial endeavor. Naringenin, a flavanone derivative, possesses anti-cancer and anti-inflammatory properties and has been reported to have cytotoxic effects on various cancer cells. The current study investigated the underlying molecular mechanism by which naringenin induces cell death in lung cancer. Methods: The expression of apoptosis, cell cycle arrest, and autophagy markers in H1299 and A459 lung cancer cells was evaluated using a terminal deoxynucleotidyl transferase dUTP nick end labeling assay (TUNEL), Western blot, Annexin V/PI stain, PI stain, acridine orange staining, and transmission electron microscopy (TEM). Using fluorescence microscopy, DALGreen was used to observe the degradation of p62, a GFP-LC3 plasmid was used to evaluate puncta formation, and a pcDNA3-GFP-LC3-RFP-LC3ΔG plasmid was used to evaluate autophagy flux. Furthermore, the anti-cancer effect of naringenin was evaluated in a subcutaneous H1299 cell xenograft model. Results: Naringenin treatment of lung cancer cells (H1299 and A459) reduced cell viability and induced cell cycle arrest. Pretreatment of cells with ROS scavengers (N-acetylcysteine or catalase) suppressed the naringenin-induced cleavage of apoptotic protein and restored cyclin-dependent kinase activity. Naringenin also triggered autophagy by mediating ROS generation, thereby activating AMP-activated protein kinase (AMPK) signaling. ROS inhibition not only inhibited naringenin-induced autophagic puncta formation but also decreased the ratio of microtubule-associated proteins 1A/1B light chain 3 II (LC3II)/LC3I and activity of the AMPK signaling pathway. Furthermore, naringenin suppressed tumor growth and promoted apoptosis in the xenograft mouse model. Conclusion: This study demonstrated the potent anti-cancer effects of naringenin on lung cancer cells, thereby providing valuable insights for developing small-molecule drugs that can induce cell cycle arrest, apoptosis, and autophagic cell death.

Acetylshikonin induces necroptosis via the RIPK1/RIPK3-dependent pathway in lung cancer.

Despite advances in therapeutic strategies, lung cancer remains the leading cause of cancer-related death worldwide. Acetylshikonin is a derivative of the traditional Chinese medicine Zicao and presents a variety of anticancer properties. However, the effects of acetylshikonin on lung cancer have not been fully understood yet. This study explored the mechanisms underlying acetylshikonin-induced cell death in non-small cell lung cancer (NSCLC). Treating NSCLC cells with acetylshikonin significantly reduced cell viability, as evidenced by chromatin condensation and the appearance of cell debris. Acetylshikonin has also been shown to increase cell membrane permeability and induce cell swelling, leading to an increase in the population of necrotic cells. When investigating the mechanisms underlying acetylshikonin-induced cell death, we discovered that acetylshikonin promoted oxidative stress, decreased mitochondrial membrane potential, and promoted G2/M phase arrest in lung cancer cells. The damage to NSCLC cells induced by acetylshikonin resembled results involving alterations in the cell membrane and mitochondrial morphology. Our analysis of oxidative stress revealed that acetylshikonin induced lipid oxidation and down-regulated the expression of glutathione peroxidase 4 (GPX4), which has been associated with necroptosis. We also determined that acetylshikonin induces the phosphorylation of receptor-interacting serine/threonine-protein kinase 1 (RIPK1)/RIPK3 and mixed lineage kinase domain-like kinase (MLKL). Treatment with RIPK1 inhibitors (necrostatin-1 or 7-Cl-O-Nec-1) significantly reversed acetylshikonin-induced MLKL phosphorylation and NSCLC cell death. These results indicate that acetylshikonin activated the RIPK1/RIPK3/MLKL cascade, leading to necroptosis in NSCLC cells. Our findings indicate that acetylshikonin reduces lung cancer cells by promoting G2/M phase arrest and necroptosis.

Exposure to incense burning, biomarkers, and the physical health of temple workers in Taiwan.

Incense burning releases heavy particulate matter (PM) and nitrogen dioxide (NO2), known to have adverse effects on human health. Long-term exposure to PM and NO2 increases inflammatory cytokine levels and can induce respiratory diseases. This study examined the association between incense burning exposure and the health status, especially inflammatory biomarkers, of temple workers and volunteers in Taiwan. The longitudinal observational study compared adult temple workers and volunteers, with long-term incense burning exposure, to residents from outpatient clinics in the Chiayi area. Forced expiratory volume in 1 s (FEV1) and serum and exhaled breath condensate (EBC) cytokines were assessed. Nonparametric Mann-Whitney U tests were used to compare cytokine levels of the exposure and control groups during the cold and hot weather seasons. FEV1 was significantly more diminished in the exposed group than in the control group during the cold season. Exposure status was associated with greater hot-cold seasonal differences in serum interleukins (IL)-1ß (regression coefficient (B) = 6.6, 95% confidence interval (CI) = 5.0 to 8.3, p < .001), IL17-A (B = 2.4, 95% CI = 0.3 to 4.5, p = .03), and plasminogen activator inhibitor [PAI]-1 (B = 5.4, 95% CI = 1.5 to 9.3, p = .009). After adjusting for confounders, the groups' serum levels of IL-1ß, IL-17A, and PAI-1 significantly differed. EBC cytokines did not show significant differences. Elevated levels of IL-1ß, IL17-A, and PAI-1 have been associated with various autoinflammatory syndromes and diseases. Given the cultural significance of incense burning, culturally sensitive interventions, including education, policy development, and program implementation, are crucial to protect individuals' health, especially temple workers, from the adverse effects of exposure, addressing the manufacture, importation, and sale of incense.

Growth, mortality, and resource utilization of Gymnocypris chui in Langcuo Lake of Tibetan Plateau, China.

To investigate the growth, mortality, and resource utilization of Gymnocypris chui in Langcuo Lake of Tibetan Plateau, we measured body length and body weight of 389 fish based on four sampling surveys from October 2018 to November 2019. We identified the ages through lapillus. Based on frequency distribution of body length, we estimated the growth and mortality coefficients of G. chui in Langcuo Lake and the utilization status of existing population resources according to the Beverton-Holt dynamic comprehensive model. The results showed that G. chui were mainly composed of individuals aged 2 to 19 years in Langcuo Lake, with a length-body weight relationship equation of W=0.0105L3.042. The von Bertalanffy growth equation revealed that the fish had an asymptotic body length of L∞=37.28 cm, growth coefficient of k=0.160, and theoretical growth starting age of t0=-0.887 a. The total mortality coefficient Z was estimated as 0.48, based on the length-converted catch curve method. According to Pauly's empirical formula, the natural mortality coefficient M was 0.34, fishing mortality coefficient F was 0.14, and exploitation rate E was 0.29, indicating that G. chui resources in Langcuo Lake were not over-exploited. Considering the growth and mortality of G. chui in Langcuo Lake, fishing is appropriate, with a recommended fishing length of Lc=22.37 cm.

Tanshinone IIA suppresses burning incense-induced oxidative stress and inflammatory pathways in astrocytes.

The burning incense (BI) behavior could be widely observed in Asia families. Incense sticks are often believed to be made from natural herbs and powders, and to have minimal impact on human health; however, there is limited research to support this claim. The current study aimed to identify the components of BI within the particulate matter 2.5 µm (PM2.5) range and explore if BI has bio-toxicity effects on rat astrocytes (CTX-TNA2). The study also examined the protective effects and underlying molecular mechanisms of tanshinone IIA, a primary lipid-soluble compound found in the herb danshen (Salvia miltiorrhiza Bunge), which has been shown to benefit the central nervous system. Results showed that despite the differences in BI components compared to the atmospheric particulate matter (PM) standards, BI still had a bio-toxicity on astrocytes. BI exposure caused early and late apoptosis, reactive oxygen species (ROS) production, MAPKs (JNK, p38, and ERK), and Akt signaling activation, and inflammation-related proteins (cPLA2, COX-2, HO-1, and MMP-9) increases. Our results further exhibit that the tanshinone IIA pre-treatment could significantly avoid the BI-induced apoptosis and inflammatory signals on rat astrocytes. These findings suggest that BI exposure may cause oxidative stress in rat astrocytes and increase inflammation-related proteins and support the potential of tanshinone IIA as a candidate for preventing BI-related adverse health effects.

CXCL14 promotes metastasis of non-small cell lung cancer through ACKR2-depended signaling pathway.

Background: Lung cancer is a malignant tumor with metastatic potential. Chemokine ligand 14 (CXCL14) has been reported to be associated with different cancer cell migration and invasion. However, few studies have explored the function of CXCL14 and its specific receptor in lung cancer metastasis. This study aims to determine the mechanism of CXCL14-promoted cancer metastasis. Methods: The expression of CXCL14, atypical chemokine receptor 2 (ACKR2), and epithelial mesenchymal transition (EMT) markers was evaluated by the public database of The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), Western blot, enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (qPCR), immunohistochemistry (IHC), and immunofluorescence (IF). Migration and wound healing assays were used to observe the motility of cancer cells. A luciferase reporter assay was performed to analyze transcription factor activity. The metastasis of lung cancer cells was evaluated in an orthotopic model. Results: We have presented that overexpression of CXCL14 and ACKR2 was observed in lung cancer datasets, human lung tumor sections, and lung cancer cells. Furthermore, the migration of CXCL14-promoted lung cancer cells was determined in vitro and in vivo. In particular, ACKR2 knockdown abolished CXCL14-induced cancer cell motility. Additionally, ACKR2 was involved in CXCL14-triggered phospholipase Cß3 (PLCß3), protein kinase Cα (PKCα), and proto-oncogene c-Src signaling pathway and subsequently upregulated nuclear factor κB (NF-κB) transcription activity leading to EMT and migration of lung cancer cells. These results indicated that the CXCL14/ACKR2 axis played an important role in lung cancer metastasis. Conclusion: This study is the first to reveal the function of CXCL14 in promoting EMT and metastasis in lung cancer. As a specific receptor for CXCL14 in lung cancer, ACKR2 mediates CXCL14-induced signaling that leads to cell motility. Our findings can be used as a prognostic biomarker of lung cancer metastasis.

N-acetylcysteine alleviates fine particulate matter (PM2.5)-induced lung injury by attenuation of ROS-mediated recruitment of neutrophils and Ly6Chigh monocytes and lung inflammation.

BACKGROUND: Exposure to particulate matter (PM) may contribute to lung inflammation and injury. The therapeutic effect of N-acetylcysteine (NAC), a well-known antioxidant, with regards to the prevention and treatment of fine PM (PM2.5)-induced lung injury is poorly understood. This study aimed to determine the effect of PM2.5 on the recruitment of neutrophils and Ly6Chigh monocytes into lung alveoli and the production of proinflammatory proteins by stimulating the generation of reactive oxygen species (ROS), and to investigate the therapeutic effect of NAC on PM2.5-induced lung injury. METHODS: C57BL/6 mice were exposed to a single administration of PM2.5 (200 µg/100 µl/mouse) or phosphate-buffered saline (control) via intratracheal instillation. The mice were injected intratracheally via a microsprayer aerosolizer with NAC (20 or 40 mg/kg) 1 h before PM2.5 instillation and 24 h after PM2.5 instillation. Total protein, VEGF, IL-6, and TNF-α in bronchoalveolar lavage fluid (BALF) were measured. Oxidative stress was evaluated by determining levels of malondialdehyde (MDA) and nitrite in BALF. Flow cytometric analysis was used to identify and quantify neutrophils and Ly6Chigh and Ly6Clow monocyte subsets. RESULTS: Neutrophil count, total protein, and VEGF content in BALF significantly increased after PM2.5 exposure and reached the highest level on day 2. Increased levels of TNF-alpha, IL-6, nitrite, and MDA in BALF were also noted. Flow cytometric analysis showed increased recruitment of neutrophils and Ly6Chigh, but not Ly6Clow monocytes, into lung alveoli. Treatment with NAC via the intratracheal spray significantly attenuated the recruitment of neutrophils and Ly6Chigh monocytes into lung alveoli in PM2.5-treated mice in a dose-dependent manner. Furthermore, NAC significantly attenuated the production of total protein, VEGF, nitrite, and MDA in the mice with PM2.5-induced lung injury in a dose-dependent manner. CONCLUSION: PM2.5-induced lung injury caused by the generation of oxidative stress led to the recruitment of neutrophils and Ly6Chigh monocytes, and production of inflammatory proteins. NAC treatment alleviated PM2.5-induced lung injury by attenuating the ROS-mediated recruitment of neutrophils and Ly6Chigh monocytes and lung inflammation.

Naringenin Induces ROS-Mediated ER Stress, Autophagy, and Apoptosis in Human Osteosarcoma Cell Lines.

Osteosarcoma, a primary bone tumor, responds poorly to chemotherapy and radiation therapy in children and young adults; hence, as the basis for an alternative treatment, this study investigated the cytotoxic and antiproliferative effects of naringenin on osteosarcoma cell lines, HOS and U2OS, by using cell counting kit-8 and colony formation assays. DNA fragmentation and the increase in the G2/M phase in HOS and U2OS cells upon treatment with various naringenin concentrations were determined by using the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay and Annexin V/propidium iodide double staining, respectively. Flow cytometry was performed, and 2',7'-dichlorodihydrofluorescein diacetate, JC-1, and Fluo-4 AM ester probes were examined for reactive oxygen species (ROS) generation, mitochondrial membrane potential, and intracellular calcium levels, respectively. Caspase activation, cell cycle, cytosolic and mitochondrial, and autophagy-related proteins were determined using western blotting. The results indicated that naringenin significantly inhibited viability and proliferation of osteosarcoma cells in a dose-dependent manner. In addition, naringenin induced cell cycle arrest in osteosarcoma cells by inhibiting cyclin B1 and cyclin-dependent kinase 1 expression and upregulating p21 expression. Furthermore, naringenin significantly inhibited the growth of osteosarcoma cells by increasing the intracellular ROS level. Naringenin induced endoplasmic reticulum (ER) stress-mediated apoptosis through the upregulation of ER stress markers, GRP78 and GRP94. Naringenin caused acidic vesicular organelle formation and increased autophagolysosomes, microtubule-associated protein-light chain 3-II protein levels, and autophagy. The findings suggest that the induction of cell apoptosis, cell cycle arrest, and autophagy by naringenin through mitochondrial dysfunction, ROS production, and ER stress signaling pathways contribute to the antiproliferative effect of naringenin on osteosarcoma cells.

A Role of CXCL1 Drives Osteosarcoma Lung Metastasis via VCAM-1 Production.

Osteosarcoma, a common aggressive and malignant cancer, appears in the musculoskeletal system among young adults. The major cause of mortality in osteosarcoma was the recurrence of lung metastases. However, the molecular mechanisms of metastasis involved in osteosarcomas remain unclear. Recently, CXCL1 and CXCR2 have been crucial indicators for lung metastasis in osteosarcoma by paracrine releases, suggesting the involvement of directing neutrophils into tumor microenvironment. In this study, overexpression of CXCL1 has a positive correlation with the migratory and invasive activities in osteosarcoma cell lines. Furthermore, the signaling pathway, CXCR2/FAK/PI3K/Akt, is activated through CXCL1 by promoting vascular cell adhesion molecule 1 (VCAM-1) via upregulation of nuclear factor-kappa B (NF-κB) expression and nuclear translocation. The in vivo animal model further demonstrated that CXCL1 serves as a critical promoter in osteosarcoma metastasis to the lung. The correlated expression of CXCL1 and VCAM-1 was observed in the immunohistochemistry staining from human osteosarcoma specimens. Our findings demonstrate the cascade mechanism regulating the network in lung metastasis osteosarcoma, therefore indicating that the CXCL1/CXCR2 pathway is a worthwhile candidate to further develop treatment schemas.

The Adverse Impact of Incense Smoke on Human Health: From Mechanisms to Implications.

Incense burning is a very popular activity in daily life among many parts all over the world. A growing body of both epidemiological and experimental evidences has reported the negative effects of incense use on human well-being, posing a potential threat at public significance. This work is a comprehensive review that covers the latest findings regarding the adverse impact of incense smoke on our health, providing a panoramic visualization ranging from mechanisms to implications. The toxicities of incense smoke come directly from its harmful constituents and deposition capacity in the body. Besides, reactive oxygen species-driven oxidative stress and associated inflammation seem to be plausible underlying mechanisms, eliciting various unfavorable responses. Although our current knowledge remains many gaps, this issue still has some important implications.

Selection of suitable reference genes for quantitative real time PCR in different Tulasnella isolates and orchid-fungus symbiotic germination system.

Under natural conditions, mycorrhizal symbiosis accompanies nearly the entire life cycle of orchids from seed germination through to flowering and fruiting. Tulasnella-like orchid mycorrhizal fungi are the most common mycorrhizal fungi found in association with orchid species. Presently suitable reference genes have not been systematically selected for the quantification of gene expression via Real-Time Quantitative Reverse Transcription PCR (RT-qPCR). We evaluated 12 candidate Tulasnella genes in nine different Tulasnella isolates and in the Dendrobium-fungal symbiotic germination associations followed by statistical analysis using the programs Bestkeeper, geNorm, and Normfinder to analyze the expression stability of the individual genes. The results showed that the EF2, UBC, and PP2A genes had the highest rankings with relatively stable expression levels across the different genotypes and during the symbiotic seed germination process by the three programs, and may be suitable for RT-qPCR normalization. Furthermore, the gene encoding C-5 Sterol desaturase (C5SD) was selected to verify the reliability of EF2, UBC, and PP2A expression during the Tulasnella-Dendrobium symbiotic seed germination process. This study is the first systematic exploration of optimal reference genes for gene expression studies during the colonization of orchid seeds by the mycorrhizal fungus Tulasnella.

PM2.5 facilitates IL-6 production in human osteoarthritis synovial fibroblasts via ASK1 activation.

Osteoarthritis (OA) is a progressive degenerative joint disorder characterized by synovial inflammation. Interleukin-6 (IL-6) is a key proinflammatory cytokine in OA progression. Particulate matter 2.5 (PM2.5) exposure increases the risk of different diseases, including OA. Up until now, no studies have described any association between PM2.5 and IL-6 expression in human OA synovial fibroblasts (OASFs). Here, our data show that PM2.5 concentration- and time-dependently promoted IL-6 synthesis in human OASFs. We also found that reactive oxygen species (ROS) generation potentiated the effects of PM2.5 on IL-6 production. ASK1, ERK, p38, and JNK inhibitors reduced PM2.5-induced increases of IL-6 expression. Treatment of OASFs with PM2.5 promoted phosphorylation of these signaling cascades. We also found that PM2.5 enhanced c-Jun phosphorylation and its translocation into the nucleus. Thus, PM2.5 increases IL-6 production in human OASFs via the ROS, ASK1, ERK, p38, JNK, and AP-1 signaling pathways. Our evidence links PM2.5 with OA progression.

CXCL1 contributes to IL-6 expression in osteoarthritis and rheumatoid arthritis synovial fibroblasts by CXCR2, c-Raf, MAPK, and AP-1 pathway.

BACKGROUND: Osteoarthritis (OA) and rheumatoid arthritis (RA) are common joint disorders that are considered to be different diseases due to their unique molecular mechanisms and pathogenesis. Chemokines and their corresponding receptors have been well characterized in RA progression, but less so in OA pathogenesis. METHODS: The human primary synovial fibroblasts (SFs) were obtained from human OA and RA tissue samples. The Western blot and qPCR were performed to analyze the expression levels of CXCL1, as well as CXCL-promoted IL-6 expression in both OASFs and RASFs. The signal cascades that mediate the CXCL1-promoted IL-6 expression were identified by using chemical inhibitors, siRNAs, and shRNAs. RESULTS: Here, we found that both diseases feature elevated levels of CXCL1 and interleukin (IL)-6, an important proinflammatory cytokine that participates in OA and RA pathogenesis. In OASFs and RASFs, CXCL1 promoted IL-6 expression in a dose- and time-dependent manner. In OASFs and RASFs overexpressing CXCL1 or transduced with shRNA plasmid, IL-6 expression was markedly upregulated. CXCR2, c-Raf, and MAPKs were found to regulate CXCL1-induced IL-6 expression in OASFs and RASFs. Finally, CXCL1 triggered the transcriptional activities of c-Jun (which regulates the expression of proinflammatory proteins) in OASFs and RASFs. CONCLUSIONS: Our present work suggests that the CXCL1/CXCR2 axis helps to orchestrate inflammatory responses in OA and RA SFs.

Contributions of burning incense on indoor air pollution levels and on the health status of patients with chronic obstructive pulmonary disease.

BACKGROUND: Among Buddhist or Taoist Taiwanese residents, burning incense is a common source of indoor particulate matter (PM), including PM10 and PM2.5, and can adversely affect the health status of patients with chronic obstructive pulmonary diseases (COPD). However, few studies have focused on the effects of intermittent burning of incense on PM concentration levels and the health status of patients with COPD. This correlational cohort study aimed to investigate the association between burning incense exposure duration, indoor air pollution levels, and lung function in patients with COPD in Taiwan. METHODS: We assessed 18 outpatients at seven time points with moderate-to-severe COPD using the COPD Assessment Test (CAT), and lung function tests. PM level changes were assessed at seven intervals using generalized estimating equations. RESULTS: Participants were primarily male (84%), with a mean age of 72.1 (standard deviation (SD)  ± 9.3) years, and with a mean COPD duration of 3.7 (SD  ± 3.1) years. Both PM10 and PM2.5 levels were the same as the background levels 1 h after incense burning. Burning incense may not influence lung function or symptom severity in patients with COPD in a short-time period. Air quality returned to baseline levels 1 h after burning incense. CONCLUSION: Patients with COPD should avoid staying in rooms where incense is burnt, for up to 1 h. The small sample size and short study period may have influenced our results. Future longitudinal studies with larger sample sizes and long-term follow-ups are recommended.

The Inducible Role of Ambient Particulate Matter in Cancer Progression via Oxidative Stress-Mediated Reactive Oxygen Species Pathways: A Recent Perception.

Cancer is one of the leading causes of premature death and overall death in the world. On the other hand, fine particulate matter, which is less than 2.5 microns in aerodynamic diameter, is a global health problem due to its small diameter but high toxicity. Accumulating evidence has demonstrated the positive associations between this pollutant with both lung and non-lung cancer processes. However, the underlying mechanisms are yet to be elucidated. The present review summarizes and analyzes the most recent findings on the relationship between fine particulate matter and various types of cancer along with the oxidative stress mechanisms as its possible carcinogenic mechanisms. Also, promising antioxidant therapies against cancer induced by this poison factor are discussed.

Arthrobacter crusticola sp. nov., Isolated from Biological Soil Crusts in the Mu Us Sandy Land, China.

Mu Us Sandy Land in China is a very fragile ecological environment due to serious desertification. While attempting to gain insights into the biodiversity of biological soil crusts of Mu Us Sandy Land, a novel bacterial strain, SLN-3T, was isolated. It was phylogenetically placed into the genus Arthrobacter within the family Micrococcaceae based on its 16S rRNA gene sequence. The most closely related species were Arthrobacter ruber MDB1-42T (98.6%) and Arthrobacter agilis DSM 20550T (98.3%). Cells of the novel species were Gram-stain-positive, aerobic, and non-endospore-forming. The values of average nucleotide identity and the digital DNA-DNA hybridization between SLN-3T and MDB1-42T were 84.9% and 21.3%, respectively. The draft genome size of strain SLN-3T was 3.67 Mb, and its genomic G+C content was 68.1%. The predominant cellular fatty acids were anteiso-C15:0 and C17:0 anteiso. Glucose, galactose, and ribose were the whole-cell sugars. The polar lipids consisted of diphosphatidylglycerol, phosphatidylglycerol, phosphatidylinositol, glycolipid, and phospholipid. The peptidoglycan contained lysine, glutamic acid, and alanine. The predominant menaquinone was MK-9(H2). Based on the data from the chemotaxonomic, phylogenetic, and phenotypic evidence, a novel species named Arthrobacter crusticola sp. nov is proposed, whose type strain is SLN-3T (= ACCC 61595T = JCM 33723T).