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Background/Aims Hyperuricemia plays an essential role in the gout. Despite the clinical significance of hyperuricemia, a direct relationship between oral health and hyperuricemia has not been established. We aim to investigate the association between oral health and hyperuricemia. Methods We selected 17,557 subjects from the Korea National Health and Nutrition Examination Survey database for the years 2016–2019. Oral health-related variables included the number of dental caries, regular tooth brushing, use of secondary oral products, and regular dental examinations. The odds ratio (OR) and 95% confidence intervals (CIs) for hyperuricemia were calculated using a multivariable-adjusted logistic regression model. Results Oral health status with dental caries and oral health behaviors, including tooth brushing, secondary oral products, and regular dental examination, were significantly associated with hyperuricemia in all participants. The adjusted OR and 95% CIs for hyperuricemia comparing more than three dental caries with no dental caries were 1.28 (1.08–1.52). The adjusted OR and 95% CIs for hyperuricemia in regular tooth brushing, use of secondary oral products, and regular dental examination were 0.78 (0.67–0.91), 0.91 (0.83–1.00), and 0.86 (0.78–0.95), respectively. Notably, the association between oral health and hyperuricemia was more prominent in male subjects. In addition, when subjects were grouped by the oral health scoring system, the prevalence of hyperuricemia was lower in groups with better oral health scores. Conclusions We demonstrated that oral health status and behaviors are associated with hyperuricemia, particularly in males. Further studies are necessary to confirm the association between oral health and hyperuricemia.

Background: Recently, open pose estimation using artificial intelligence (AI) has enabled the analysis of time series of human movements through digital video inputs. Analyzing a person's actual movement as a digitized image would give objectivity in evaluating a person's physical function. In the present study, we investigated the relationship of AI camera-based open pose estimation with Harris Hip Score (HHS) developed for patient-reported outcome (PRO) of hip joint function. Method: HHS evaluation and pose estimation using AI camera were performed for a total of 56 patients after total hip arthroplasty in Gyeongsang National University Hospital. Joint angles and gait parameters were analyzed by extracting joint points from time-series data of the patient's movements. A total of 65 parameters were from raw data of the lower extremity. Principal component analysis (PCA) was used to find main parameters. K-means cluster, X-squared test, Random forest, and mean decrease Gini (MDG) graph were also applied. Results: The train model showed 75% prediction accuracy and the test model showed 81.8% reality prediction accuracy in Random forest. “Anklerang_max”, “kneeankle_diff”, and “anklerang_rl” showed the top 3 Gini importance score in the Mean Decrease Gini (MDG) graph. Conclusion: The present study shows that pose estimation data using AI camera is related to HHS by presenting associated gait parameters. In addition, our results suggest that ankle angle associated parameters could be key factors of gait analysis in patients who undergo total hip arthroplasty.

Abstract Background In the emergency room, clinicians spend a lot of time and are exposed to mental stress. In addition, fracture classification is important for determining the surgical method and restoring the patient's mobility. Recently, with the help of computers using artificial intelligence (AI) or machine learning (ML), diagnosis and classification of hip fractures can be performed easily and quickly. The purpose of this systematic review is to search for studies that diagnose and classify for hip fracture using AI or ML, organize the results of each study, analyze the usefulness of this technology and its future use value. Methods PubMed Central, OVID Medline, Cochrane Collaboration Library, Web of Science, EMBASE, and AHRQ databases were searched to identify relevant studies published up to June 2022 with English language restriction. The following search terms were used [All Fields] AND (", "[MeSH Terms] OR (""[All Fields] AND "bone"[All Fields]) OR "bone fractures"[All Fields] OR "fracture"[All Fields]). The following information was extracted from the included articles: authors, publication year, study period, type of image, type of fracture, number of patient or used images, fracture classification, reference diagnosis of fracture diagnosis and classification, and augments of each studies. In addition, AI name, CNN architecture type, ROI or important region labeling, data input proportion in training/validation/test, and diagnosis accuracy/AUC, classification accuracy/AUC of each studies were also extracted. Results In 14 finally included studies, the accuracy of diagnosis for hip fracture by AI was 79.3–98%, and the accuracy of fracture diagnosis in AI aided humans was 90.5–97.1. The accuracy of human fracture diagnosis was 77.5–93.5. AUC of fracture diagnosis by AI was 0.905–0.99. The accuracy of fracture classification by AI was 86–98.5 and AUC was 0.873–1.0. The forest plot represented that the mean AI diagnosis accuracy was 0.92, the mean AI diagnosis AUC was 0.969, the mean AI classification accuracy was 0.914, and the mean AI classification AUC was 0.933. Among the included studies, the architecture based on the GoogLeNet architectural model or the DenseNet architectural model was the most common with three each. Among the data input proportions, the study with the lowest training rate was 57%, and the study with the highest training rate was 95%. In 14 studies, 5 studies used Grad-CAM for highlight important regions. Conclusion We expected that our study may be helpful in making judgments about the use of AI in the diagnosis and classification of hip fractures. It is clear that AI is a tool that can help medical staff reduce the time and effort required for hip fracture diagnosis with high accuracy. Further studies are needed to determine what effect this causes in actual clinical situations.

Accelerated global warming is leading to the loss of plant species diversity, and ex situ preservation of seeds is becoming an increasingly important aspect of species conservation. However, information on dormancy and germination is lacking in many endangered species. Amsonia elliptica (Apocynaceae) is the only Amsonia species native to Korea, and the South Korean Ministry of Environment has designated it Class II endangered wildlife. Nevertheless, the dormancy class and the dormancy breaking method for seeds of this species for germination are not precisely known. We identified the structure of A. elliptica seeds and the causes of dormancy, which inhibits germination. In addition, we tried to develop an effective germination promotion method by testing the wet stratified condition, which breaks dormancy, and the form of gibberellin that can replace it. Fresh seeds of A. elliptica imbibe water, but the covering layers (endosperm and seed coat) inhibit germination by mechanically restricting the embryo. Initial germination tests confirmed low embryo growth potential and physiological dormancy (PD). Restriction due to the covering layer was eliminated by seed scarification, and abnormal germination was observed. After 12 weeks of cold moist stratification at 4°C, only 12% of seeds germinated. However, 68.8% of seeds subjected to 8 weeks of warm moist stratification followed by 12 weeks of cold stratification germinated, indicating that warm stratification pretreatment before cold stratification is effective in breaking dormancy. A. elliptica seeds exhibited intermediate PD. Furthermore, 61.3% of seeds soaked in 500 mg/L GA4+7 for 14 days and incubated at 25/15°C germinated. Therefore, GA4+7 rapidly broke the dormancy of A. elliptica seeds compared with warm plus cold stratification treatment, thus providing an efficient method for seedling production.

This study aimed to investigate the effect of light [a long-day photoperiod (16 h light/8 h dark cycle)] and dark treatment on the production of rosmarinic acid in P. frutescens microgreens and to determine its antioxidant and antibacterial activities. Microgreens of P. frutescens were grown under light and dark conditions and harvested after 10, 15, 20, and 25 days of each treatment. Although dry weight values of microgreens gradually increased from 10 to 25 days of both treatments, the microgreens grown under light treatment possessed slightly higher levels of dry weight than those grown in the dark. Rosmarinic acid and total phenolic content (TPC) were also analyzed using high-performance liquid chromatography (HPLC) and Folin–Ciocalteu assay. The accumulation patterns of rosmarinic acid and TPC gradually increased and decreased, respectively, in P. frutescens microgreens grown in continuous darkness. The highest accumulation was observed in microgreens grown for 20 days. However, rosmarinic acid and TPC values were not significantly different in microgreens grown under light conditions. According to the 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical inhibition assay, the extracts of P. frutescens microgreens were confirmed to be strong antioxidants, and their ability to scavenge DPPH radicals was positively correlated with the total phenolic content in the microgreens after 10, 15, 20, and 25 days of both treatments. Considering the relatively higher values of dry weight, rosmarinic acid, TPC, and DPPH assay, P. frutescens microgreens after 20 days of darkness and 20 days of light treatment, respectively, were selected for screening antibacterial activity using nine pathogens. Both microgreen extracts showed strong antibacterial activity against pathogens. In particular, the extracts of microgreens grown for 20 days under light treatment showed higher antimicrobial effects. Therefore, the light treatments for 20 days, as well as the darkness treatment for 20 days, were the best conditions for P. frutescens microgreen production because of their high levels of dry weight, phenolics, and biological activities.

Gom-chwi (Ligularia fischeri) is severely infected with Phytophthora drechsleri, the causal organism of Phytophthora root rot, an economically important crop disease that needs management throughout the cultivation period. In the present study, Phytophthora root rot was controlled by using bacterial isolates from rhizosphere soils collected from various plants and screened for antagonistic activity against P. drechsleri. A total of 172 bacterial strains were isolated, of which, 49 strains showed antagonistic activities by dual culture assay. In the seedling assay, six out of the 49 strains showed a predominant effect on suppressing P. drechsleri. Among the six strains, the ObRS-5 strain showed remarkable against P. drechsleri when treated with seed dipping or soil drenching. The ObRS-5 strain was identified as Enterobacter asburiae based on 16S ribosomal RNA gene sequences analysis. The bacterial cells of E. asburiae ObRS-5 significantly suppressed sporangium formation and zoospore germination in P. drechsleri by 87.4% and 66.7%, respectively. In addition, culture filtrate of E. asburiae ObRS-5 also significantly inhibited sporangium formation and zoospore germination by 97.0% and 67.6%, respectively. Soil drenched bacterial cells, filtrate, and culture solution of E. asburiae ObRS-5 effectively suppressed Phytophthora root rot by 63.2%, 57.9%, and 81.1%, respectively. Thus, E. asburiae ObRS-5 could be used as a potential agent for the biological control of Phytophthora root rot infecting gom-chwi.

One of the causes of sarcopenia is that homeostasis between anabolism and catabolism breaks down due to muscle metabolism changes. Rutin has shown antioxidant and anti-inflammatory effects in various diseases, but there are few studies on the effect on muscle loss with aging. The effect of rutin on muscle loss was evaluated using dexamethasone-induced muscle loss C2C12 myoblast and mouse model. In the group treated with dexamethasone, the muscle weight of gastrocnemius (GA), tibialis anterior (TA), and extensor digitorum longus (EDL) in the mouse model were significantly decreased (p < 0.0001 in GA, p < 0.0001 in TA, and p < 0.001 in EDL) but recovered (p < 0.01 in GA, p < 0.0001 in TA, and p < 0.01 in EDL) when treated with rutin. MAFbx, MuRF1, and FOXO3 protein expression of C2C12 myoblast were significantly increased (p < 0.01 in MAFbx, p < 0.01 in MuRF1, and p < 0.01 in FOXO3) when treated with dexamethasone, but it was recovered (p < 0.01 in MAFbx, p < 0.01 in MuRF1, and p < 0.01 in FOXO3) when rutin was treated. In addition, MAFbx and FOXO3 protein expression in GA of mouse model was significantly increased (p < 0.0001 in MAFbx and p < 0.001 in FOXO3) when treated with dexamethasone, but it was also recovered (p < 0.01 in MAFbx and p < 0.001 in FOXO3) when rutin was treated. The present study shows that rutin blocks the FOXO3/MAFbx and FOXO3/MuRf1 pathways to prevent protein catabolism. Therefore, rutin could be a potential agent for muscle loss such as sarcopenia through the blocking ubiquitin-proteasome pathway associated with catabolic protein degradation.

Diet digestibility can vary based on factors such as the type of ingredients, processing techniques, formulation, fiber content, and nutrient interactions. Unlike proteins and fats, there is no specific carbohydrate requirement, which typically constitutes 30%–60% of commercial dried dog foods. Because of the significant proportion of carbohydrates in dog food, this study aimed to evaluate the differences in nutrient digestibility among barley, brown rice, corn, mung bean, and rice, which are common carbohydrate sources in commercial dog foods. All experimental diets had consistent chemical compositions. The digestibility of each carbohydrate source was evaluated using the total feces collection method in four castrated male and four neutered female beagles with an average age of 4.58 ± 0.14 years. The average daily dry matter intake of the five experimental diets was 203.0 ± 3.23 g/day. The percentage of dry matter digestibility of the apparent total tract digestibility (ATTD) was the highest for rice and corn at 92.45% and 92.95%, respectively, followed by brown rice (91.61%), barley (88.81%), and mung beans (80.74%). The percentage of nitrogen-free extract digestibility was also high for rice, corn, and brown rice at 97.08%, 96.14%, and 95.56%, respectively, followed by barley at 90.10% and mung bean at 83.38%. Amino acid digestibility analysis revealed no statistically significant differences between rice, corn, brown rice, and barley, except for methionine, which is an essential amino acid. Although the ATTD and amino acid profile of the mung bean-based diet were less efficient than those of the other test diets, the overall digestibility was satisfactory and there were no significant differences in palatability. The differences in digestibility observed in mung bean-based diets compared to other grain-based diets can be attributed to variations in the starch and fiber content of the raw materials. By leveraging these characteristics, mung bean-based diets may offer strategic benefits for glycemic control and weight management in dogs. Our results may serve as a basis for formulating appropriate diets for dogs.

Macrophages are crucially involved in the pathogenesis of rheumatoid arthritis (RA). Macrophages of the M1 phenotype act as pro-inflammatory mediators in synovium, whereas those of the M2 phenotype suppress inflammation and promote tissue repair. SIRT1 is a class 3 histone deacetylase with anti-inflammatory characteristics. However, the role played by SIRT1 in macrophage polarization has not been defined in RA. We investigated whether SIRT1 exerts anti-inflammatory effects by modulating M1/M2 polarization in macrophages from RA patients. In this study, SIRT1 activation promoted the phosphorylation of an adenosine monophosphate-activated protein kinase (AMPK) α/acetyl-CoA carboxylase in macrophages exposed to interleukin (IL)-4, and that this resulted in the expressions of M2 genes, including MDC, FcεRII, MrC1, and IL-10, at high levels. Furthermore, these expressions were inhibited by sirtinol (an inhibitor of SIRT1) and compound C (an inhibitor of AMPK). Moreover, SIRT1 activation downregulated LPS/interferon γ-mediated NF-κB activity by inhibiting p65 acetylation and the expression of M1 genes, such as CCL2, iNOS, IL-12 p35, and IL-12 p40. Macrophages from SIRT1 transgenic (Tg)-mice exhibited enhanced polarization of M2 phenotype macrophages and reduced polarization of M1 phenotype macrophages. In line with these observations, SIRT1-Tg mice showed less histological signs of arthritis, that is, lower TNFα and IL-1β expressions and less severe arthritis in the knee joints, compared to wild-type mice. Taken together, the study shows activation of SIRT1/AMPKα signaling exerts anti-inflammatory activities by regulating M1/M2 polarization, and thereby reduces inflammatory responses in RA. Furthermore, it suggests that SIRT1 signaling be viewed as a therapeutic target in RA.

This paper describes a novel chromatographic method for efficient removal of anionic dyes from aqueous solutions. Chitosan-coated Fe3O4 nanoparticles can easily be immobilized on a dextran gel column. Single elution of Evans Blue (EB) solution to the nanoadsorbent-incorporated columns provides high removal efficiency with a maximum adsorption capacity of 243.9 mg/g. We also investigated the influence of initial concentration and solution pH on the removal efficiency of EB. The electrostatic interaction between the adsorbent surface and negatively charged sulfate groups on EB molecules promotes the efficient adsorption of dyes. The equilibrium data matched well with the Langmuir isotherm model, which indicated monolayer dye adsorption onto the adsorbent surface. To extend the application of the current method, we performed further adsorption experiments using other anionic dyes of different colors (Cy5.5, Acid Yellow 25, Acid Green 25, and Acid Red 1). All of these molecules can efficiently be captured under continuous flow conditions, with higher removal efficiency obtained with more negatively charged dyes. These findings clearly demonstrate that the present approach is a useful method for the removal of anionic dye contaminants in aqueous media by adsorption.

Although alpha (α)B-crystallin is expressed in articular chondrocytes, little is known about its role in these cells. Protein kinase casein kinase 2 (CK2) inhibition induces articular chondrocyte death. The present study examines whether αB-crystallin exerts anti-apoptotic activity in articular chondrocytes. Primary rat articular chondrocytes were isolated from knee joint slices. Cells were treated with CK2 inhibitors with or without αB-crystallin siRNA. To examine whether the silencing of αB-crystallin sensitizes rat articular chondrocytes to CK2 inhibition-induced apoptosis, we assessed apoptosis by performing viability assays, mitochondrial membrane potential measurements, flow cytometry, nuclear morphology observations, and western blot analysis. To investigate the mechanism by which αB-crystallin modulates the extent of CK2 inhibition-mediated chondrocyte death, we utilized confocal microscopy to observe the subcellular location of αB-crystallin and its phosphorylated forms and performed a co-immunoprecipitation assay to observe the interaction between αB-crystallin and CK2. Immunochemistry was employed to examine αB-crystallin expression in cartilage obtained from rats with experimentally induced osteoarthritis (OA). Our results demonstrated that silencing of αB-crystallin sensitized rat articular chondrocytes to CK2 inhibitor-induced apoptosis. Furthermore, CK2 inhibition modulated the expression and subcellular localization of αB-crystallin and its phosphorylated forms and dissociated αB-crystallin from CK2. The population of rat articular chondrocytes expressing αB-crystallin and its phosphorylated forms was reduced in an experimentally induced rat model of OA. In summary, αB-crystallin protects rat articular chondrocytes against CK2 inhibition-induced apoptosis. αB-crystallin may represent a suitable target for pharmacological interventions to prevent OA.

Background: Self-expanding metal and plastic esophageal stents (SEMS and SEPS, respectively) are used in conjunction with chemoradiation for palliation of malignant dysphagia. To date, the dosimetric effects of stents undergoing proton radiotherapy are not known. Study aim: To investigate the proton radiotherapy dose perturbations caused by esophageal stents of varying designs and materials undergoing external beam treatment for esophageal cancer. Patients and methods: Simulated clinical protocol. Solid acrylic phantom was used to mimic the esophageal tissue environment. Stents made of nitinol, stainless steel and polyester were tested. Proton beam dose of 2 Gy-E was delivered to each stent in a single anterior to posterior field. Film and image based evidence of dose perturbation were main outcomes measured. Results: Only the stainless steel and plastic stents demonstrated slight overall dose attenuations (– 0.5 % and – 0.4 %, respectively). All the nitinol-based stents demonstrated minimal overall dose perturbations ranging from 0.0 % to 1.2 %. Negligible dose perturbations were observed on each of the stent surfaces proximal to the radiation source, ranging from – 0.8 % (stainless steel stent) to 1.0 % (nitinol stent). Negligible dose effects were also observed on the distal surfaces of each stent ranging from – 0.5 % (plastic and stainless steel stents) to 1.0 % (nitinol stent). Conclusion: Proton radiotherapy dose perturbations caused by stents of varying designs and material composition are negligible. Negligible dose perturbation is in keeping with the inherent advantage of proton therapy over traditional radiotherapy composed of photons – given its relative large mass, protons have little side scatter.

Despite the numerous studies of protein kinase CK2, little progress has been made in understanding its function in chondrocyte death. Our previous study first demonstrated that CK2 is involved in apoptosis of rat articular chondrocytes. Recent studies have suggested that CK2 downregulation is associated with aging. Thus examining the involvement of CK2 downregulation in chondrocyte death is an urgently required task. We undertook this study to examine whether CK2 downregulation modulates chondrocyte death. We first measured CK2 activity in articular chondrocytes of 6-, 21- and 30-month-old rats. Noticeably, CK2 activity was downregulated in chondrocytes with advancing age. To build an in vitro experimental system for simulating tumor necrosis factor (TNF)-α-induced cell death in aged chondrocytes with decreased CK2 activity, chondrocytes were co-treated with CK2 inhibitors and TNF-α. Viability assay demonstrated that CK2 inhibitors facilitated TNF-α-mediated chondrocyte death. Pulsed-field gel electrophoresis, nuclear staining, flow cytometry, TUNEL staining, confocal microscopy, western blot and transmission electron microscopy were conducted to assess cell death modes. The results of multiple assays showed that this cell death was mediated by apoptosis. Importantly, autophagy was also involved in this process, as supported by the appearance of a punctuate LC3 pattern and autophagic vacuoles. The inhibition of autophagy by silencing of autophage-related genes 5 and 7 as well as by 3-methyladenine treatment protected chondrocytes against cell death and caspase activation, indicating that autophagy led to the induction of apoptosis. Autophagic cells were observed in cartilage obtained from osteoarthritis (OA) model rats and human OA patients. Our findings indicate that CK2 down regulation facilitates TNF-α-mediated chondrocyte death through apoptosis and autophagy. It should be clarified in the future if autophagy observed is a consequence versus a cause of the degeneration in vivo.