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Background: Particulate matter of less than 2.5 micrometers (PM2.5) is associated with various adverse health outcomes. Limited evidence exists however regarding the effects of the individual constituents of indoor PM2.5 and whether their concentrations are affected by the environment or lifestyle. We here investigated the associations between these individual constituents and respiratory outcomes, the living environment, and daily life behaviors in patients with chronic obstructive pulmonary disease (COPD). Methods: This was a prospective panel study involving COPD patients recruited from three hospitals in the Republic of Korea. Detailed questionnaires on living environments and lifestyle practices were completed by the participants. Associations between indoor PM2.5 constituents and respiratory outcomes, living environments, and daily life behaviors were then analyzed. Correlation analyses were conducted using a Spearman’s rank-order or Pearson’s correlation. Results: A total of 89 stable COPD cases were included. Their mean age was 68.1 years and 84 (94.4%) were men. The median indoor PM2.5 concentration was 11.3 μg/m3. Titanium was significantly associated with small airway resistance. Higher concentrations of aluminum, bromine, and silicone correlated with more frequent exacerbations. Regarding the living environment, the copper concentrations were negatively correlated with the distance from a road and with the floor level of residence. A higher manganese concentration was associated with greater traffic volume. An increased ventilation time was associated with lower concentrations of copper and silicone, whereas the air purifier operation time on a day with a heavy dust level was negatively correlated with barium and titanium concentrations. Iron and manganese were negatively correlated with a frequency of cleaning the kitchen ventilator. Conclusion: PM2.5 comprises various chemical constituents, each showing different relationships with clinical parameters in patients with COPD. Such constituents may be affected by environmental factors or lifestyles and should be considered as part of individualized intervention strategies through further studies.

Excessive hepatic glucose production (HGP) is a key factor promoting hyperglycemia in diabetes. Hepatic cryptochrome 1 (CRY1) plays an important role in maintaining glucose homeostasis by suppressing forkhead box protein O1 (FOXO1)-mediated HGP. Although downregulation of hepatic CRY1 appears to be associated with increased HGP, the mechanism(s) by which hepatic CRY1 dysregulation confers hyperglycemia in diabetic subjects is largely unknown. In this study, we demonstrate that a reduction in hepatic CRY1 protein is stimulated by elevated E3 ligase F-box and leucine-rich repeat protein 3 (FBXL3)-dependent proteasomal degradation in diabetic mice. In addition, we found that GSK3b-induced CRY1 phosphorylation potentiates FBXL3-dependent CRY1 degradation in the liver. Accordingly, in diabetic mice, GSK3b inhibitors effectively decreased HGP by facilitating the effect of CRY1-mediated FOXO1 degradation on glucose metabolism. Collectively, these data suggest that tight regulation of hepatic CRY1 protein stability is crucial for maintaining systemic glucose homeostasis.

Skin antiseptics have important implications for public health and medicine. Although conventional antiseptics have considerable antimicrobial activity, skin toxicity and the development of resistance are common problems. Plasma-treated water has sterilization and tissue-regenerative effects. Therefore, the aim of this study was to identify whether plasma-activated water (PAW) manufactured by our microwave plasma system can be used as a novel antiseptic solution for skin protection. PAW was produced by dissolving reactive nitrogen oxide gas using microwave plasma in deionized water. The antibacterial effects of PAW against Staphylococcus aureus, Escherichia coli, Pseudomonas aeruginosa, Bacillus cereus, and Salmonella typhimurium and effective concentrations were investigated by a solid agar plate assay. The factors mediating the effects of PAW were evaluated by the addition of reactive species scavengers. Cytotoxicity and cell viability assays were performed to examine the protective effect of PAW on normal skin cells. PAW exhibited excellent sterilization and no toxicity in normal skin cells. Experiments also confirmed the potential of PAW as a sanitizer for SARS-CoV-2. Our findings support the use of PAW as an effective skin disinfectant with good safety in the current situation of a global pandemic.

Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease and is strongly associated with obesity-related ectopic fat accumulation in the liver. Hepatic lipid accumulation encompasses a histological spectrum ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), which can progress to cirrhosis and hepatocellular carcinoma. Given that dysregulated hepatic lipid metabolism may be an onset factor in NAFLD, understanding how hepatic lipid metabolism is modulated in healthy subjects and which steps are dysregulated in NAFLD subjects is crucial to identify effective therapeutic targets. Additionally, hepatic inflammation is involved in chronic hepatocyte damage during NAFLD progression. As a key immune signaling hub that mediates NF-κB activation, the IκB kinase (IKK) complex, including IKKα, IKKβ, and IKKγ (NEMO), has been studied as a crucial regulator of the hepatic inflammatory response and hepatocyte survival. Notably, TANK-binding kinase 1 (TBK1), an IKK-related kinase, has recently been revealed as a potential link between hepatic inflammation and energy metabolism. Here, we review (1) the biochemical steps of hepatic lipid metabolism; (2) dysregulated lipid metabolism in obesity and NAFLD; and (3) the roles of IKKs and TBK1 in obesity and NAFLD., Obesity: tracing the inflammation underlying liver disease A deeper understanding of the molecular processes underlying dysfunctional fatty-acid metabolism in nonalcoholic fatty liver disease (NAFLD) could help protect patients from severe liver damage. NAFLD is a common consequence of obesity, and severe disease can ultimately give rise to liver cancer or cirrhosis. Alan Saltiel of the University of California, San Diego, USA, and Jin Young Huh of Seoul National University, South Korea, have reviewed current knowledge of the mechanisms governing fatty acid metabolism in the liver, and how they are disturbed in obesity and NAFLD. The various IκB kinase (IKK) complexes and a protein known as TANK-binding kinase 1 (TBK1) play particularly prominent roles in the inflammatory response associated with NAFLD pathogenesis. Better insights into IKK- and TBK1-associated regulatory pathways could inform the development of new interventions for this currently untreatable condition.

In mammals, brown adipose tissue (BAT) is specialized to conduct non-shivering thermogenesis for survival under cold acclimation. Although emerging evidence suggests that lipid metabolites are essential for heat generation in cold-activated BAT, the underlying mechanisms of lipid uptake in BAT have not been thoroughly understood. Here, we show that very-low-density lipoprotein (VLDL) uptaken by VLDL receptor (VLDLR) plays important roles in thermogenic execution in BAT. Compared with wild-type mice, VLDLR knockout mice exhibit impaired thermogenic features. Mechanistically, VLDLR-mediated VLDL uptake provides energy sources for mitochondrial oxidation via lysosomal processing, subsequently enhancing thermogenic activity in brown adipocytes. Moreover, the VLDL-VLDLR axis potentiates peroxisome proliferator activated receptor (PPAR)β/δ activity with thermogenic gene expression in BAT. Accordingly, VLDL-induced thermogenic capacity is attenuated in brown-adipocyte-specific PPARβ/δ knockout mice. Collectively, these data suggest that the VLDL-VLDLR axis in brown adipocytes is a key factor for thermogenic execution during cold exposure.

Adipose tissue dysfunction is a hallmark of obesity and contributes to obesity-related sequelae such as metabolic complications and insulin resistance. Compelling evidence indicates that adipose-tissue-specific gene expression is influenced by gene interactions with proximal and distal cis-regulatory elements; the latter exert regulatory effects via three-dimensional (3D) chromosome conformation. Recent advances in determining the regulatory mechanisms reveal that compromised epigenomes are molecularly interlinked to altered cis-regulatory element activity and chromosome architecture in the adipose tissue. This review summarizes the roles of epigenomic components, particularly DNA methylation, in transcriptional rewiring in adipose tissue. In addition, we discuss the emerging roles of DNA methylation in the maintenance of 3D chromosome conformation and its pathophysiological significance concerning adipose tissue function.

Macrophage proinflammatory activation is an important etiologic component of the development of insulin resistance and metabolic dysfunction in obesity. However, the underlying mechanisms are not clearly understood. Here, we demonstrate that a mitochondrial inner membrane protein, adenine nucleotide translocase 2 (ANT2), mediates proinflammatory activation of adipose tissue macrophages (ATMs) in obesity. Ant2 expression was increased in ATMs of obese mice compared with lean mice. Myeloid-specific ANT2-knockout (ANT2-MKO) mice showed decreased adipose tissue inflammation and improved insulin sensitivity and glucose tolerance in HFD/obesity. At the molecular level, we found that ANT2 mediates free fatty acid-induced mitochondrial permeability transition, leading to increased mitochondrial reactive oxygen species production and damage. In turn, this increased HIF-1α expression and NF-κB activation, leading to proinflammatory macrophage activation. Our results provide a previously unknown mechanism for how obesity induces proinflammatory activation of macrophages with propagation of low-grade chronic inflammation (metaflammation).

RATIONALE Chronic obstructive lung disease (COPD) is a chronic progressive disease. Although smoking is the most important risk factor, 30% of COPD patients are never smokers, and environmental age...

Background Recent study suggested that combination therapy with pirfenidone and nintedanib had a manageable safety and tolerability profile in patients with idiopathic pulmonary fibrosis (IPF). However, safety and efficacy of combination therapy in real-world practice are unknown. We aimed to investigate safety and efficacy of combination therapy with pirfenidone and add-on nintedanib in patients with IPF. Methods Clinical data of IPF patients treated with pirfenidone and add-on nintedanib were retrospectively analyzed. Adverse events and lung function declines were compared before and after treatment with nintedanib. Results Nineteen patients with IPF underwent combination therapy. At the beginning of treatment, the mean age of all patients was 70.4 years and 84.2% were male. The median follow-up period was 7.6 months. All patients received add-on nintedanib during treatment with pirfenidone at a stable dose (mean dose: 1768.4 ± 137.6 mg/day, mean duration 32.0 ± 11.2 months ). Most common adverse events attributable to nintedanib were diarrhea (31.6%), anorexia (21.1%) and dyspepsia (15.8%). In 3 patients (15.6%), one of the antifibrotic agents was discontinued due to adverse events (pirfenidone in 2, and nintedanib in 1 due to anorexia or dyspepsia). In 13 patients with serial lung function data before and after treatment, decline rate in forced vital capacity (FVC) significantly reduced (-12.4 ± 2.0 ml/month [before] vs. -10 ± 4.6 ml/month [after], p < 0.001) after treatment with nintedanib. Decline in FVC for 3 months also significantly reduced (-154 mL [before] vs. 93 mL [after], p=0.002) after treatment (Figure 1). Conclusions Our data suggests that the combination therapy with pirfenidone and add-on nintedanib had a manageable safety profile, and might be more effective than monotherapy

The mechanisms by which macrophages regulate energy storage remain poorly understood. We identify in a genetic screen a PDGF-family growth factor, Pvf3, produced by macrophages that is required for lipid storage in fat body cells of Drosophila larvae. Genetic and pharmacological experiments indicate that the mouse Pvf3 ortholog, PDGFcc, produced by adipose-tissue resident macrophages controls lipid storage in adipocytes in a Leptin- and Ccr2- independent manner. PDGFcc production is regulated by diet, and acts in a paracrine manner to control lipid storage in adipose tissues of newborn and adult mice. At the organismal level upon PDGFcc blockade, excess lipids are redirected toward thermogenesis in brown fat. These data identify a macrophage-dependent mechanism, conducive to the design of pharmacological interventions, that controls energy storage in metazoans.

The purpose of this study is to investigate the effect of Grit on career decision making self-efficacy and career preparation behaviors of university students in physical education. The purpose of this study is to examine the effect of Grit on university students in physical education in Seoul and Gyeonggido. The data were analyzed by frequency, factor analysis, correlation analysis, regression analysis, and structural equation modeling using SPSS 21.0 program and AMOS 21.0 program. Based on the results and discussions, the following conclusions were obtained. First, all variables such as steady effort and continuous interest, which are sub-factors of Grit, had a positive influence on all of the sub-factors of career decision making self-efficacy, such as goal selection, future planning and job information. These results indicate that Grit is a very important variable to enhance career decision making self-efficacy. Second, all variables such as steady effort and continuous interest, which are sub-factors of Grit, had a positive influence on career exploration behavior, information gathering behavior, and job experience behavior. These results indicate that Grit is a very important variable for enhancing career preparation behavior. Third, all variables such as goal selection, future plan, and job information, which are sub-factors of career decision making self-efficacy, have positive significance in career exploration behavior, information gathering behavior, It affected. These results indicate that career decision making self-efficacy of university students is a very important variable to enhance career preparation behavior. Fourth, the relationship among Grit, career decision making self-efficacy and career preparation behavior was confirmed, and it was confirmed that there was a positive causality between each variables.

We report a simple method for the synthesis of hydrogenated TiO2 (H-TiO2) by submerging an atmospheric-pressure plasma jet in a titanium precursor solution. The synthesized H-TiO2 demonstrates improved visible light absorption and electrical conductivity due to a decreased work function and narrowed band gap. Our plasma system has significant benefits compared to previously reported hydrogenation methods. It offers a facile, one-pot synthesis process, rapid synthesis time, and ease of mass production. We expect the plasma system to be a promising technology for the synthesis of H-TiO2, and believe this method has potential for use in new environmental and optoelectronic applications.

Decreased adipose tissue oxygen tension and increased HIF-1α expression can trigger adipose tissue inflammation and dysfunction in obesity. Our current understanding of obesity-associated decreased adipose tissue oxygen tension is mainly focused on changes in oxygen supply and angiogenesis. Here, we demonstrate that increased adipocyte O2 demand, mediated by ANT2 activity, is the dominant cause of adipocyte hypoxia. Deletion of adipocyte Ant2 improves obesity-induced intracellular adipocyte hypoxia by decreasing obesity-induced adipocyte oxygen demand, without effects on mitochondrial number or mass, or oligomycin-sensitive respiration. This led to decreased adipose tissue HIF-1α expression and inflammation with improved glucose tolerance and insulin resistance in both a preventative or therapeutic setting. Our results suggest that ANT2 may be a target for the development of insulin sensitizing drugs and that ANT2 inhibition might have clinical utility.

White adipose tissue (WAT) is a key regulator of systemic energy metabolism, and impaired WAT plasticity characterized by enlargement of preexisting adipocytes associates with WAT dysfunction, obesity, and metabolic complications. However, the mechanisms that retain proper adipose tissue plasticity required for metabolic fitness are unclear. Here, we comprehensively showed that adipocyte-specific DNA methylation, manifested in enhancers and CTCF sites, directs distal enhancer-mediated transcriptomic features required to conserve metabolic functions of white adipocytes. Particularly, genetic ablation of adipocyte Dnmt1, the major methylation writer, led to increased adiposity characterized by increased adipocyte hypertrophy along with reduced expansion of adipocyte precursors (APs). These effects of Dnmt1 deficiency provoked systemic hyperlipidemia and impaired energy metabolism both in lean and obese mice. Mechanistically, Dnmt1 deficiency abrogated mitochondrial bioenergetics by inhibiting mitochondrial fission and promoted aberrant lipid metabolism in adipocytes, rendering adipocyte hypertrophy and WAT dysfunction. Dnmt1-dependent DNA methylation prevented aberrant CTCF binding and, in turn, sustained the proper chromosome architecture to permit interactions between enhancer and dynamin-1-like protein gene Dnm1l (Drp1) in adipocytes. Also, adipose DNMT1 expression inversely correlated with adiposity and markers of metabolic health but positively correlated with AP-specific markers in obese human subjects. Thus, these findings support strategies utilizing Dnmt1 action on mitochondrial bioenergetics in adipocytes to combat obesity and related metabolic pathology.

Adipose tissue macrophages (ATMs) have important roles in the regulation of inflammatory responses and insulin resistance in obesity. A new study reports that a subpopulation of ATMs, TIM4+ resident ATMs, modulate adipocyte size via platelet-derived growth factor-CC production during development and diet-induced adipose tissue expansion.

Accumulating evidence reveals that adipose tissue is an immunologically active organ that exerts multiple impacts on the regulation of systemic energy metabolism. Adipose tissue immunity is modulated by the interactions between adipocytes and various immune cells. Nevertheless, the underlying mechanisms that control inter-cellular interactions between adipocytes and immune cells in adipose tissue have not been thoroughly elucidated. Recently, it has been demonstrated that adipocytes utilize lipid metabolites as a key mediator to initiate and mediate diverse adipose tissue immune responses. Adipocytes present lipid antigens and secrete lipid metabolites to determine adipose immune tones. In addition, the interactions between adipocytes and adipose immune cells are engaged in the control of adipocyte fate and functions upon metabolic stimuli. In this review, we discuss an integrated view of how adipocytes communicate with adipose immune cells using lipid metabolites. Also, we briefly discuss the newly discovered roles of adipose stem cells in the regulation of adipose tissue immunity.

In mammals, white adipose tissues are largely divided into visceral epididymal adipose tissue (EAT) and subcutaneous inguinal adipose tissue (IAT) with distinct metabolic properties. Although emerging evidence suggests that subpopulations of adipose stem cells (ASCs) would be important to explain fat depot differences, ASCs of two fat depots have not been comparatively investigated. Here, we characterized heterogeneous ASCs and examined the effects of intrinsic and tissue micro-environmental factors on distinct ASC features. We demonstrated that ASC subpopulations in EAT and IAT exhibited different molecular features with three adipogenic stages. ASC transplantation experiments revealed that intrinsic ASC features primarily determined their adipogenic potential. Upon obesogenic stimuli, EAT-specific SDC1

Numerous reports have elucidated that TiO2 nanoparticles (TiO2-NPs) exhibit respectable photocatalytic degradation capacities due to their high specific surface areas. However, the current recovery process leads to a loss of TiO2-NPs; therefore, there is a need to immobilize TiO2-NPs on the substrate used. Herein, TiO2-coated yttria-stabilized zirconia/silica nanofiber (TiO2-coated YSZ/silica NF) was prepared by coating TiO2 on the surface of YSZ/silica NF using a sol–gel process. The TiO2 coating layer on the nanofiber surface improved the separation ability of the membrane as well as the photocatalytic degradation ability. The pore size of the TiO2-coated YSZ/silica NF membrane was less than that of the pristine YSZ/silica NF membrane, and it rejected over 99.6% of the 0.5 μm polymeric particles. In addition, the TiO2-coated YSZ/silica NF membrane showed excellent adsorption/degradation of humic acid (HA, 88.2%), methylene blue (MB, 92.4%), and tetracycline (TC, 99.5%). Six recycling tests were performed to evaluate the reusability of the TiO2-coated YSZ/silica NF membrane. The adsorption/degradation efficiency for HA, MB, and TC decreased by 3.7%, 2.8%, and 2.2%, respectively. We thus verified the high separation ability, excellent photocatalytic degradation ability, and excellent reusability of the TiO2-coated YSZ/silica NF membranes.

Numerous reports have elucidated that TiO2 nanoparticles (TiO2-NPs) exhibit respectable photocatalytic degradation capacities due to their high specific surface areas. However, the current recovery process leads to a loss of TiO2-NPs; therefore, there is a need to immobilize TiO2-NPs on the substrate used. Herein, TiO2-coated yttria-stabilized zirconia/silica nanofiber (TiO2-coated YSZ/silica NF) was prepared by coating TiO2 on the surface of YSZ/silica NF using a sol–gel process. The TiO2 coating layer on the nanofiber surface improved the separation ability of the membrane as well as the photocatalytic degradation ability. The pore size of the TiO2-coated YSZ/silica NF membrane was less than that of the pristine YSZ/silica NF membrane, and it rejected over 99.6% of the 0.5 μm polymeric particles. In addition, the TiO2-coated YSZ/silica NF membrane showed excellent adsorption/degradation of humic acid (HA, 88.2%), methylene blue (MB, 92.4%), and tetracycline (TC, 99.5%). Six recycling tests were performed to evaluate the reusability of the TiO2-coated YSZ/silica NF membrane. The adsorption/degradation efficiency for HA, MB, and TC decreased by 3.7%, 2.8%, and 2.2%, respectively. We thus verified the high separation ability, excellent photocatalytic degradation ability, and excellent reusability of the TiO2-coated YSZ/silica NF membranes.

Foreign body aspiration can produce a medical emergency. Obstruction of the airways can be life-threatening, and complications may develop in less-severe cases if it is left untreated. Although it is more prevalent in children by approximately three times, adults can still experience it, and it is more frequently related to healthcare in adults. Objects used in dental treatment are usually placed in the oral cavity and can be ingested or inhaled by accident. Dental treatment has been identified as an important cause of the misplacement of foreign bodies in the airway. However, few reports have been published on dentistry-related foreign body aspiration. This paper discusses the disease course, management, and clinical outcomes of foreign body aspiration, especially those associated with dentistry. The patient must be examined for respiratory distress. If the patient is unstable, urgent airway management and the maneuvers for removal should be performed. Radiographs and computed tomography can help identify and locate the object. The treatment of choice is often bronchoscopy, and both flexible and rigid endoscopes can be used depending on the situation. Preventive measures need to be implemented to avoid inhalation accidents given the potential consequences. Though the incidence is rare, healthcare levels need to be enhanced to avert morbidity and mortality. Radiological evaluation and bronchoscopy are vital for management.

In this paper, it is first reported that gray hydrogenated TiO2 sphere photocatalysts (H-TiO2) with high reactivity to solar light are mass produced within a few minutes using an underwater discharge plasma modified sol-gel method at room temperature and atmospheric pressure. This plasma modified system is an easy one-step in-situ synthetic process and the crystallinity, hydrogenation, and spherical structure of H-TiO2 are achieved by the synergy effect between the continuous reaction of highly energetic atomic and molecular species generated from the underwater plasma and surface tension of water. The resultant H-TiO2 demonstrated high anatase/rutile bicrystallinity and extended optical absorption spectrum from the ultraviolet (UV) to visible range. Furthermore, various defects including oxygen vacancies and hydroxyl species on the TiO2 surface permitted the enhancement of the photocatalytic performance. It was demonstrated that H-TiO2 photocatalysts showed significant degradation efficiencies for reactive black 5 (RB 5), rhodamine B (Rho B), and phenol (Ph) under solar light irradiation, up to approximately 5 times higher than that of commercial anatase TiO2 (C-TiO2), which resulted in good water purification. Notably, it was also possible to cultivate HepG2 cells using such well-purified water (to degrees up to 76%), with minimal cytotoxicity. Considering all these results, we believe that this novel plasma technology is promising for important environmental applications.

In obesity, adipose tissue undergoes dynamic remodeling processes such as adipocyte hypertrophy, hypoxia, immune responses, and adipocyte death. However, whether and how invariant natural killer T (iNKT) cells contribute to adipose tissue remodeling are elusive. In this study, we demonstrate that iNKT cells remove unhealthy adipocytes and stimulate the differentiation of healthy adipocytes. In obese adipose tissue, iNKT cells were abundantly found nearby dead adipocytes. FasL-positive adipose iNKT cells exerted cytotoxic effects to eliminate hypertrophic and pro-inflammatory Fas-positive adipocytes. Furthermore, in vivo adipocyte-lineage tracing mice model showed that activation of iNKT cells by alpha-galactosylceramide promoted adipocyte turnover, eventually leading to potentiation of the insulin-dependent glucose uptake ability in adipose tissue. Collectively, our data propose a novel role of adipose iNKT cells in the regulation of adipocyte turnover in obesity.

In this study, we propose a meshless scheme, GC-LSM (Geometric Conservation Least Squares Method), satisfying the geometric conservation and 1st order consistency. These constraints are introduced in order to overcome the non-conservativeness of the original meshless scheme and imposed by Lagrange multiplier on the least squares method which determines weighting coefficients of the derivative terms. Improvements on the meshless scheme are confirmed through computations with randomly distributed grid points for a sine wave, nozzle flow, and hypersonic flow around blunt body. Combined with AUSMPW + and MUSCL scheme, GC-LSM of the second order accuracy gives non-oscillating solution around a strong shockwave, even for hypersonic flow, and shows its capability comparable to the finite volume method in views of accuracy, robustness, and convergence.

Introduction: Chronic obstructive pulmonary disease (COPD) is commonly affected by particulate matter (PM) exposure. In this study, we aimed to evaluate whether behavioral interventions to reduce PM exposure improve clinical outcomes in patients with COPD. Methods: A multicenter randomized controlled trial will be conducted involving 120 participants recruited from 3 hospitals in the capital region of the Republic of Korea. Patients aged 40 to 80 years with a diagnosis of COPD and a forced expiratory volume at 1 s

In this paper, we report on the mass production, characteristics and application of a hydrogenated TiO 2 photocatalyst (H-TiO 2 ) with high reactivity under solar light irradiation. The H-TiO 2 photocatalyst has been prepared by simple sol-gel method/underwater discharge plasma treatment at room temperature and atmospheric pressure. The optical absorption spectrum of TiO 2 can be extended from the ultraviolet (UV) into the visible range by changing the surface properties. The crystallinity, hydrogenation and porosity of TiO 2 can be greatly enhanced within 90 s through underwater discharge plasma, using amorphous TiO 2 (as-synthesized TiO 2 , a-TiO 2 ) as the precursor. The resultant H-TiO 2 showed high bicrystalline (anatase/brookite phases) and a large surface area (267.5 m 2 /g), thus improving photocatalytic activity. We have demonstrated that H-TiO 2 showed significant photocatalytic efficiencies for degradation of reactive black 5, rhodamine B, and phenol under solar light irradiation, up to 10 times higher than those of commercial TiO 2 and a-TiO 2 , leading to complete water purification. Interestingly, the H-TiO 2 photocatalyst also exhibited strong antimicrobial activities against Gram-negative Escherichia coli and Gram-positive Staphylococcus aureus under solar light irradiation, up to 5-times greater than those of commercial TiO 2 and a-TiO 2 . Given that H-TiO 2 can be mass produced and easily processed by underwater discharge plasma, we expect this plasma technology may find important environmental and medical applications.