This review article explores the multifaceted relationship between air pollution and interstitial lung diseases (ILDs), particularly focusing on idiopathic pulmonary fibrosis, the most severe form of fibrotic ILD. Air pollutants are mainly composed of particulate matter, ozone (O3), nitrogen dioxide (NO2), carbon monoxide (CO), and sulfur dioxide (SO2). They are recognized as risk factors for several respiratory diseases. However, their specific effects on ILDs and related mechanisms have not been thoroughly studied yet. Emerging evidence suggests that air pollutants may contribute to the development and acute exacerbation of ILDs. Longitudinal studies have indicated that air pollution can adversely affect the prognosis of disease by decreasing lung function and increasing mortality. Lots of in vitro, in vivo , and epidemiologic studies have proposed possible mechanisms linking ILDs to air pollution, including inflammation and oxidative stress induced by exposure to air pollutants, which may induce mitochondrial dysfunction, promote cellular senescence, and disrupt normal epithelial repair processes. Despite these findings, effective interventions to mitigate effects of air pollution on ILD are not well established yet. This review emphasizes the urgent need to address air pollution as a key environmental risk factor for ILDs and calls for further studies to clarify its effects and develop preventive and therapeutic strategies.

This review article explores the multifaceted relationship between air pollution and interstitial lung diseases (ILDs), particularly focusing on idiopathic pulmonary fibrosis, the most severe form of fibrotic ILD. Air pollutants are mainly composed of particulate matter, ozone (O3), nitrogen dioxide (NO2), carbon monoxide (CO), and sulfur dioxide (SO2). They are recognized as risk factors for several respiratory diseases. However, their specific effects on ILDs and related mechanisms have not been thoroughly studied yet. Emerging evidence suggests that air pollutants may contribute to the development and acute exacerbation of ILDs. Longitudinal studies have indicated that air pollution can adversely affect the prognosis of disease by decreasing lung function and increasing mortality. Lots of in vitro, in vivo , and epidemiologic studies have proposed possible mechanisms linking ILDs to air pollution, including inflammation and oxidative stress induced by exposure to air pollutants, which may induce mitochondrial dysfunction, promote cellular senescence, and disrupt normal epithelial repair processes. Despite these findings, effective interventions to mitigate effects of air pollution on ILD are not well established yet. This review emphasizes the urgent need to address air pollution as a key environmental risk factor for ILDs and calls for further studies to clarify its effects and develop preventive and therapeutic strategies.

This review article explores the multifaceted relationship between air pollution and interstitial lung diseases (ILDs), particularly focusing on idiopathic pulmonary fibrosis, the most severe form of fibrotic ILD. Air pollutants are mainly composed of particulate matter, ozone (O3), nitrogen dioxide (NO2), carbon monoxide (CO), and sulfur dioxide (SO2). They are recognized as risk factors for several respiratory diseases. However, their specific effects on ILDs and related mechanisms have not been thoroughly studied yet. Emerging evidence suggests that air pollutants may contribute to the development and acute exacerbation of ILDs. Longitudinal studies have indicated that air pollution can adversely affect the prognosis of disease by decreasing lung function and increasing mortality. Lots of in vitro, in vivo , and epidemiologic studies have proposed possible mechanisms linking ILDs to air pollution, including inflammation and oxidative stress induced by exposure to air pollutants, which may induce mitochondrial dysfunction, promote cellular senescence, and disrupt normal epithelial repair processes. Despite these findings, effective interventions to mitigate effects of air pollution on ILD are not well established yet. This review emphasizes the urgent need to address air pollution as a key environmental risk factor for ILDs and calls for further studies to clarify its effects and develop preventive and therapeutic strategies.

This review article explores the multifaceted relationship between air pollution and interstitial lung diseases (ILDs), particularly focusing on idiopathic pulmonary fibrosis, the most severe form of fibrotic ILD. Air pollutants are mainly composed of particulate matter, ozone (O3), nitrogen dioxide (NO2), carbon monoxide (CO), and sulfur dioxide (SO2). They are recognized as risk factors for several respiratory diseases. However, their specific effects on ILDs and related mechanisms have not been thoroughly studied yet. Emerging evidence suggests that air pollutants may contribute to the development and acute exacerbation of ILDs. Longitudinal studies have indicated that air pollution can adversely affect the prognosis of disease by decreasing lung function and increasing mortality. Lots of in vitro, in vivo , and epidemiologic studies have proposed possible mechanisms linking ILDs to air pollution, including inflammation and oxidative stress induced by exposure to air pollutants, which may induce mitochondrial dysfunction, promote cellular senescence, and disrupt normal epithelial repair processes. Despite these findings, effective interventions to mitigate effects of air pollution on ILD are not well established yet. This review emphasizes the urgent need to address air pollution as a key environmental risk factor for ILDs and calls for further studies to clarify its effects and develop preventive and therapeutic strategies.

This review article explores the multifaceted relationship between air pollution and interstitial lung diseases (ILDs), particularly focusing on idiopathic pulmonary fibrosis, the most severe form of fibrotic ILD. Air pollutants are mainly composed of particulate matter, ozone (O3), nitrogen dioxide (NO2), carbon monoxide (CO), and sulfur dioxide (SO2). They are recognized as risk factors for several respiratory diseases. However, their specific effects on ILDs and related mechanisms have not been thoroughly studied yet. Emerging evidence suggests that air pollutants may contribute to the development and acute exacerbation of ILDs. Longitudinal studies have indicated that air pollution can adversely affect the prognosis of disease by decreasing lung function and increasing mortality. Lots of in vitro, in vivo , and epidemiologic studies have proposed possible mechanisms linking ILDs to air pollution, including inflammation and oxidative stress induced by exposure to air pollutants, which may induce mitochondrial dysfunction, promote cellular senescence, and disrupt normal epithelial repair processes. Despite these findings, effective interventions to mitigate effects of air pollution on ILD are not well established yet. This review emphasizes the urgent need to address air pollution as a key environmental risk factor for ILDs and calls for further studies to clarify its effects and develop preventive and therapeutic strategies.

A protruding mass was identified in the papilla of the right kidney of a 10-week-old male Sprague-Dawley rat. Microscopically, the neoplastic tissues were consisted of epithelial elements, where basophilic neoplastic cells displayed a high nucleus-to-cytoplasm ratio and formed tubular growth patterns characterized by small, elongated, or convoluted tubules.Blastemal elements were often arranged in aggregates or nests, composed of tightly packed basophilic polygonal to spindloid primitive cells. The surrounding interstitial tissue appeared loose and myxomatous. Based on these histological features, the diagnosis was nephroblastoma. Nephroblastoma is considered as an embryonic tumor originated from metanephric blastemal elements in the renal cortex and typically displays characteristic triphasic patterns.Also, this tumor seldom arises from or remains localized to the renal pelvis. To our literaturereview, this is the first nephroblastoma occurred at renal papilla in a rat.

A protruding mass was identified in the papilla of the right kidney of a 10-week-old male Sprague-Dawley rat. Microscopically, the neoplastic tissues were consisted of epithelial elements, where basophilic neoplastic cells displayed a high nucleus-to-cytoplasm ratio and formed tubular growth patterns characterized by small, elongated, or convoluted tubules.Blastemal elements were often arranged in aggregates or nests, composed of tightly packed basophilic polygonal to spindloid primitive cells. The surrounding interstitial tissue appeared loose and myxomatous. Based on these histological features, the diagnosis was nephroblastoma. Nephroblastoma is considered as an embryonic tumor originated from metanephric blastemal elements in the renal cortex and typically displays characteristic triphasic patterns.Also, this tumor seldom arises from or remains localized to the renal pelvis. To our literaturereview, this is the first nephroblastoma occurred at renal papilla in a rat.

Systemic sclerosis is an autoimmune disease characterized by inflammatory reactions and fibrosis. Myofibroblasts are considered therapeutic targets for preventing and reversing the pathogenesis of fibrosis in systemic sclerosis. Although the mechanisms that differentiate into myofibroblasts are diverse, transforming growth factor β (TGF-β) is known to be a key mediator of fibrosis in systemic sclerosis. This study investigated the effects of extracellular vesicles derived from human adipose stem cells (ASC-EVs) in an in vivo systemic sclerosis model and in vitro TGF-β1-induced dermal fibroblasts. The therapeutic effects of ASC-EVs on the in vivo systemic sclerosis model were evaluated based on dermal thickness and the number of α-smooth muscle actin (α-SMA)-expressing cells using hematoxylin and eosin staining and immunohistochemistry. Administration of ASC-EVs decreased both the dermal thickness and α-SMA expressing cell number as well as the mRNA levels of fibrotic genes, such as Acta2, Ccn2, Col1a1 and Comp. Additionally, we discovered that ASC-EVs can decrease the expression of α-SMA and CTGF and suppress the TGF-β pathway by inhibiting the activation of SMAD2 in dermal fibroblasts induced by TGF-β1. Finally, TGF-β1-induced dermal fibroblasts underwent selective death through ASC-EVs treatment. These results indicate that ASC-EVs could provide a therapeutic approach for preventing and reversing systemic sclerosis.

Purpose: This study aims to explore the relationship between soy food consumption and gastric cancer (GC) risk, accounting for Helicobacter pylori infection status. Materials and Methods: We analyzed data from patients with GC and healthy individuals prospectively enrolled by 6 hospitals between 2016 and 2018. Dietary intake was evaluated using questionnaires that categorized seven dietary habits and 19 food groups. Multivariate logistic regression models were applied to examine associations. Model I adjusted for various epidemiological factors, while Model II included further adjustments for H. pylori infection.Primary exposures examined were consumption frequencies of nonfermented, unsalted soy foods (soybean/tofu) and fermented, salty soy foods (soybean paste stew). Results: A total of 5,535 participants were included, with 1,629 diagnosed with GC. In Model I, the frequency of soybean/tofu consumption was inversely related to GC risk; adjusted odd ratios (aORs) were 0.62 (95% confidence interval [CI], 0.48–0.8), 0.38 (95% CI, 0.3–0.49), 0.42 (95% CI, 0.33–0.53), and 0.33 (95% CI, 0.27–0.42) for 1 time/week, 2 times/week, 3 times/week, and ≥4 times/week. Consumption of 2 servings/week of soybean paste stew showed the lowest GC association, forming a V-shaped curve. Both low (aOR, 4.03; 95% CI, 3.09–5.26) and high serving frequencies of soybean paste stew (aOR, 2.23; 95% CI, 1.76–2.82) were associated with GC. The association between soy foods and GC in Model II was similar to that in Model I. The soy food-GC associations were consistent across sexes in Model I.Nonetheless, the positive correlation between frequent consumption of soybean paste stew (≥5 times/week) and GC was more pronounced in women (aOR, 7.58; 95% CI, 3.20–17.99) compared to men (aOR, 3.03; 95% CI, 1.61–5.88) in Model II. Subgroup analyses by H. pylori status and salty diet revealed a consistent inverse relationship between soybean/tofu and GC risk. In contrast, soybean paste stew showed a V-shaped relationship in H. pylori-positive or salty diet groups and no significant association in the H. pylori-negative group. Conclusions Soybean/tofu intake is consistently associated with a decreased risk of GC.However, the relationship between soybean paste stew consumption and GC risk varies, depending on H. pylori infection status and dietary salt intake.

A protruding mass was identified in the papilla of the right kidney of a 10-week-old male Sprague-Dawley rat. Microscopically, the neoplastic tissues were consisted of epithelial elements, where basophilic neoplastic cells displayed a high nucleus-to-cytoplasm ratio and formed tubular growth patterns characterized by small, elongated, or convoluted tubules.Blastemal elements were often arranged in aggregates or nests, composed of tightly packed basophilic polygonal to spindloid primitive cells. The surrounding interstitial tissue appeared loose and myxomatous. Based on these histological features, the diagnosis was nephroblastoma. Nephroblastoma is considered as an embryonic tumor originated from metanephric blastemal elements in the renal cortex and typically displays characteristic triphasic patterns.Also, this tumor seldom arises from or remains localized to the renal pelvis. To our literaturereview, this is the first nephroblastoma occurred at renal papilla in a rat.