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Words can convey subtle cultural stereotypes and perpetuate subconscious gender biases. Wording in job advertisements that appeals to 1 gender and deters others may unintentionally skew the applicant pool and affect the early phase of the recruitment process. "Masculine" tone can lead to decreased interest among women applicants while 'feminine' wording may not affect a man's decision to apply for the job. In this study, we evaluated the presence and extent of subtle gender bias in job advertisements for radiology faculty positions.All job postings for faculty radiologists were retrieved from the American College of Radiology Career Center website in July 2020. The complete job advertisement was analyzed using Gender Decoder, a publicly available web-based application, to determine number and percentage of female or male coded words and the overall tone of the ad. The job posts were also stratified by subspecialty, leadership positions and academic versus private practice environments.Of the 623 job postings reviewed, a little over half (52.0%) of job postings were feminine coded, 26.6% had a masculine tone and 21.3% had a neutral tone. Of the leadership (division director) positions, 50.0% (4/8) had a masculine tone, 37.5% had a feminine tone, and 12.5% had a neutral tone. Among various specialties, pediatric radiology had the lowest percentage of job posts with a masculine tone (10.5%) while nuclear medicine had the highest percentage (41.7%). The most commonly used feminine words were: "support," "responsible," "commitment" and the most common masculine words were: "competitive," "leader," "active."Most of the imaging job advertisements were feminine coded, with masculine tone in overall 26.6% posts and neutral tone in about a fifth. Leadership posts had a higher percentage of masculine tone. Awareness of these biases is important to enable diversity in recruitment and to ensure a diverse applicant pool.

Please see the Editorial Comment by Jonathan L. Mezrich discussing this article. Background: In community settings, radiologists commonly function as multispecialty radiologists, interpreting exami...

A brain-computer interface (BCI) is a system that translates brain activity into commands to operate technology. A common design for an electroencephalogram (EEG) BCI relies on the classification of the P300 event-related potential (ERP), which is a response elicited by the rare occurrence of target stimuli among common non-target stimuli. Few existing ERP classifiers directly explore the underlying mechanism of the neural activity. To this end, we perform a novel Bayesian analysis of the probability distribution of multi-channel real EEG signals under the P300 ERP-BCI design. We aim to identify relevant spatial temporal differences of the neural activity, which provides statistical evidence of P300 ERP responses and helps design individually efficient and accurate BCIs. As one key finding of our single participant analysis, there is a 90% posterior probability that the target ERPs of the channels around visual cortex reach their negative peaks around 200 milliseconds post-stimulus. Our analysis identifies five important channels (PO7, PO8, Oz, P4, Cz) for the BCI speller leading to a 100% prediction accuracy. From the analyses of nine other participants, we consistently select the identified five channels, and the selection frequencies are robust to small variations of bandpass filters and kernel hyper-parameters.

PURPOSE: To determine the impact of prolapsed volume on regurgitant volume (RegV), regurgitant fraction (RF), and left ventricular ejection fraction (LVEF) in patients with mitral valve prolapse (MVP) using cardiac MRI. MATERIALS AND METHODS: Patients with MVP and mitral regurgitation who underwent cardiac MRI from 2005 to 2020 were identified retrospectively from the electronic record. RegV is the difference between left ventricular stroke volume (LVSV) and aortic flow. Left ventricular end-systolic volume (LVESV) and LVSV were obtained from volumetric cine images, with prolapsed volume inclusion (LVESVp, LVSVp) and exclusion (LVESVa, LVSVa) providing two estimates of RegV (RegVp, RegVa), RF (RFp, RFa), and LVEF (LVEFa, LVEFp). Interobserver agreement for LVESVp was assessed using intraclass correlation coefficient (ICC). RegV was also calculated independently using measurements from mitral inflow and aortic net flow phase-contrast imaging as the reference standard (RegVg). RESULTS: The study included 19 patients (mean age, 28 years ± 16 [SD]; 10 male patients). Interobserver agreement for LVESVp was high (ICC, 0.98; 95% CI: 0.96, 0.99). Prolapsed volume inclusion resulted in higher LVESV (LVESVp: 95.4 mL ± 34.7 vs LVESVa: 82.4 mL ± 33.8; P < .001), lower LVSV (LVSVp: 100.5 mL ± 33.8 vs LVSVa: 113.5 mL ± 35.9; P < .001), and lower LVEF (LVEFp: 51.7% ± 5.7 vs LVEFa: 58.6% ± 6.3; P < .001). RegV was larger in magnitude when prolapsed volume was excluded (RegVa: 39.4 mL ± 21.0 vs RegVg: 25.8 mL ± 22.8; P = .02), with no evidence of a difference when including prolapsed volume (RegVp: 26.4 mL ± 16.4 vs RegVg: 25.8 mL ± 22.8; P > .99). CONCLUSION: Measurements that included prolapsed volume most closely reflected mitral regurgitation severity, but inclusion of this volume resulted in a lower LVEF. Keywords: Cardiac, MRI © RSNA, 2023 See also commentary by Lee and Markl in this issue.

PurposeTo demonstrate Dynamic Contrast-Enhanced (DCE) perfusion changes in brain metastasis patients after chemoradiation therapy within the treatment responders (true-response group and pseudoprogression group) and between the true-response and pseudoprogression groups.Materials and Methods38 true-response patients with 38 brain metastases (13 melanoma, 11 lung, 7 breast, 7 others) with 3 consecutive DCE-MRI examinations (pretreatment, first follow-up and second follow-up) and 7 pseudoprogression patients with 10 melanoma metastases with 2 consecutive DCE-MRI examinations (pretreatment, first follow-up) were evaluated. DCE-MRI parameters and permeability graphs increase (rapid, slow, medium) and course pattern (washout, plateau, persistent) were analyzed and compared between the timing of the examinations and between the true-response and pseudoprogression groups, using paired t-tests and Mann-Whitney U-tests as appropriate. Automatic assessment of washout curves by Olea Brain Software was reviewed.ResultsPretreatment mean wash-in (15.3±24.7 vs 6.50±14.2, P4±18×104vs 5×104±10×104, PConclusionWash-in, Vp, Ktrans, peak enhancement, AUC values in DCE perfusion were significantly decreased after chemoradiation therapy in the responders. No statistically significant difference was shown between the true-response and pseudoprogression groups on either pre-or post-treatment, indicating the homogeneous permeability profiles in the responders.

Osteoarthritis (OA) is a common degenerative joint disease characterized by an imbalance of cartilage extracellular matrix (ECM) breakdown and anabolism. Melatonin (MT) is one of the hormones secreted by the pineal gland of the brain and has anti-inflammatory, antioxidant, and anti-aging functions. To explore the role of MT in rats, we established an OA model in rats by anterior cruciate ligament transection (ACLT). Safranin O-fast green staining showed that intraperitoneal injection of MT (30 mg/kg) could alleviate the degeneration of articular cartilage in ACLT rats. Immunohistochemical (IHC) analysis found that MT could up-regulate the expression levels of collagen type II and Aggrecan and inhibit the expression levels of matrix metalloproteinase-3 (MMP-3), matrix metalloproteinase-13 (MMP-13), and ADAM metallopeptidase with thrombospondin type 1 motif 4 (ADAMTS-4) in ACLT rats. To elucidate the mechanism of MT in protecting the ECM in inflammatory factor-induced rat chondrocytes, we conducted in vitro experiments by co-culturing MT with a culture medium. Western blot (WB) showed that MT could promote the expression levels of transforming growth factor-beta 1 (TGF-β1)/SMAD family member 2 (Smad2) and sirtuin 2-related enzyme 1 (SIRT1) and inhibit the expression of levels of phosphorylated nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibi-tor (p-p65) and phosphorylated IκB kinase-α (p-IκBα). In addition, WB and real-time PCR (qRT-PCR) results showed that MT could inhibit the expression levels of MMP-3, MMP-13, ADAMTS-4, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) in chondrocytes induced by interleukin-1β (IL-1β), and up-regulate the expression of chondroprotective protein type II collagen. We found that in vivo, MT treatment protected articular cartilage in the rat ACLT model. In IL-1β-induced rat chondrocytes, MT could reduce chondrocyte matrix degradation by up-regulating nuclear factor-kB (NF-κB) signaling pathway-dependent expression of SIRT1 and protecting chondrocyte by activating the TGF-β1/Smad2 pathway.

Puerarin is an isoflavone isolated from the medicinal plant Pueraria lobata. The purpose of this study was to study the antiinflammatory and antimatrix-degrading effects of puerarin in a rat osteoarthritis (OA) model and its protective effects on joints. The rat OA model was established by anterior cruciate ligament transection (ACLT) surgery. Rats (n = 40) were divided into nontreated OA, OA + celecoxib (2.86 mg/kg), OA + puerarin (50 and 100 mg/kg), and control groups. Two weeks after surgical induction, puerarin was administered by gavage daily for 8 weeks. After 8 weeks, macroscopic observation and histopathological images showed that cartilage damage was reduced after puerarin and celecoxib treatment, the intensity of Safranin O staining was high, and the OARSI scores were significantly reduced compared to the OA group. Puerarin reduced the expression of MMP-3, MMP-13, ADAMTS-5, and COX-2 in the cartilage tissue of ACLT rats, inhibited the production of IL-1β, IL-6, and TNF-α inflammatory factors, increased Type II collagen content, and altered the expression of serum OA cartilage degradation/bone turnover biomarkers (CTX-I, CTX-II, COMP, and PIINP). Based on these findings, we speculate that puerarin supplement to attain recovery from OA damage.

Background Digital breast tomosynthesis (DBT) helps reduce recall rates and improve cancer detection compared with two-dimensional (2D) mammography but has a longer interpretation time. Purpose To evaluate the effect of DBT slab thickness and overlap on reader performance and interpretation time in the absence of 1-mm slices. Materials and Methods In this retrospective HIPAA-compliant multireader study of DBT examinations performed between August 2013 and July 2017, four fellowship-trained breast imaging radiologists blinded to final histologic findings interpreted DBT examinations by using a standard protocol (10-mm slabs with 5-mm overlap, 1-mm slices, synthetic 2D mammogram) and an experimental protocol (6-mm slabs with 3-mm overlap, synthetic 2D mammogram) with a crossover design. Among the 122 DBT examinations, 74 mammographic findings had final histologic findings, including 31 masses (26 malignant), 20 groups of calcifications (12 malignant), 18 architectural distortions (15 malignant), and five asymmetries (two malignant). Durations of reader interpretations were recorded. Comparisons were made by using receiver operating characteristic curves for diagnostic performance and paired t tests for continuous variables. Results Among 122 women, mean age was 58.6 years ± 10.1 (standard deviation). For detection of malignancy, areas under the receiver operating characteristic curves were similar between protocols (range, 0.83-0.94 vs 0.84-0.92; P ≥ .63). Mean DBT interpretation time was shorter with the experimental protocol for three of four readers (reader 1, 5.6 minutes ± 1.7 vs 4.7 minutes ± 1.4 [P < .001]; reader 2, 2.8 minutes ± 1.1 vs 2.3 minutes ± 1.0 [P = .001]; reader 3, 3.6 minutes ± 1.4 vs 3.3 minutes ± 1.3 [P = .17]; reader 4, 4.3 minutes ± 1.0 vs 3.8 minutes ± 1.1 [P ≤ .001]), with 72% reduction in both mean number of images and mean file size (P < .001 for both). Conclusion A digital breast tomosynthesis reconstruction protocol that uses 6-mm slabs with 3-mm overlap, without 1-mm slices, had similar diagnostic performance compared with the standard protocol and led to a reduced interpretation time for three of four readers. © RSNA, 2020 See also the editorial by Chang in this issue.

Altering the food intake, exercise, and sleep patterns have a great influence on the homeostasis of the biological clock. This leads to accelerated aging of the articular cartilage, susceptibility to arthropathy and other aspects. Deficiency or overexpression of certain circadian clock-related genes accelerates the cartilage deterioration and leads to phenotypic variation in different joints. The process of joint cartilage development includes the formation of joint site, interzone, joint cavitation, epiphyseal ossification center, and cartilage maturation. The mechanism by which, biological clock regulates the cell-cycle, growth, metabolism, and other biological processes of chondrocytes is poorly understood. Here, we summarized the interaction between biological clock proteins and developmental pathways in chondrogenesis and provided the evidence from other tissues that further predicts the molecular patterns of these protein-protein networks in activation, proliferation, and differentiation. The purpose of this review is to gain deeper understanding of the evolution of cartilage and its irreversibility seen in damage and aging.

Background Xylazole (Xyl) is a veterinary anesthetic that is structurally and functionally similar to xylazine. However, the effects of Xyl in vitro remain unknown. Objectives This study aimed to investigate the anesthetic mechanism of Xyl using fetal rat nerve cells treated with Xyl. Methods Fetal rat nerve cells cultured for seven days were treated with 10, 20, 30, and 40 μg/ mL Xyl for 0, 5, 10, 15, 20, 25, 30, 45, 60, 90, and 120 min. Variations of amino acid neurotransmitters (AANTs), Nitric oxide-Cyclic GMP (NO-cGMP) signaling pathway, and ATPase were evaluated. Results Xyl decreased the levels of cGMP and NO in nerve cells. Furthermore, Xyl affected the AANT content and Na+-K+-ATPase and Ca2+-Mg2+-ATPase activity in nerve cells. These findings suggested that Xyl inhibited the NO-cGMP signaling pathway in nerve cells in vitro. Conclusions This study provided new evidence that the anesthetic and analgesic effects of Xyl are related to the inhibition of the NO-cGMP signaling pathway.

Osteoarthritis (OA) substantially reduces the quality of life of the elderly. OA therapy remains a challenge since no treatment options for its causes are so far available. Over recent years, researchers have speculated that emodin may represent a potential treatment strategy for OA. However, it remains unclear whether the mechanism of action of emodin is associated with the inhibition of OA-induced oxidative stress. In the present study, the potential antioxidant mechanism of action of emodin and its protective properties against the development of OA were investigated both in vitro and in vivo. In vitro, emodin inhibited the production of reactive oxygen species (ROS) in chondrocytes induced by hydrogen peroxide (H2O2) and reduced the expression of matrix metalloproteinase (MMP)3 and MMP13 in a concentration-dependent manner. It was found that emodin upregulated the Nrf2/NQO1/HO-1 pathway, thereby attenuating the effects of oxidative stress caused by OA. In a rat model of posttraumatic OA induced by anterior cruciate ligament transection (ACLT), emodin reduced the extent of joint swelling. Emodin attenuated oxidative damage in the cartilage by upregulating superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) activity, reducing malondialdehyde (MDA) concentration and inhibiting the expression of the extracellular matrix (ECM) degradation biomarkers cartilage oligomeric matrix protein (COMP), and C-terminal telopeptide of type I collagen (CTX-I) and type II collagen (CTX-II), thereby reducing cartilage damage. In summary, the present study indicates that emodin reduces ECM degradation and oxidative stress in chondrocytes via the Nrf2/NQO1/HO-1 pathway, thereby ameliorating OA in rats.

Baicalein has been shown to have chondroprotective potential in vitro. However, its effect on disease modification in osteoarthritis (OA) is largely unknown. The present study is aimed at determining whether baicalein could slow the progression of OA and inhibit OA-related inflammation in a rat model of destabilization of the medial meniscus (DMM) and the underlying mechanisms. The rats subjected to DMM surgery were treated with baicalein (0.8, 1.6, and 3.2 μg/L, 50 μL, once a week) by intra-articular injection for 6 weeks. Dexamethasone (0.4 mg/mL, 50 μL, once a week) was used as a positive control. Histologic grading of cartilage degeneration was performed using the Osteoarthritis Research Society International (OARSI) recommended grading system (on a scale of 0-6). The expression levels of molecules associated with cartilage homeostasis and inflammatory cytokines were analyzed; moreover, the NLRP3 inflammasome activation and cartilage oxidative stress-associated molecules were determined. Baicalein treatment reduced the OARSI score and slowed OA disease progression in a dose-dependent manner within a certain range. Compared with DMM rats, intra-articular injection of baicalein led to (1) reduced levels of inflammatory mediates such as IL-1β and TNF-α, (2) reduced immunochemical staining of MMP-13 and ADAMTS-5, (3) suppressed immunochemical staining loss of type II collagen, (4) reduced expression of cartilage degradation markers including CTX-II and COMP in urine, and (5) inhibited NLRP3 inflammasome activation rather than regulated expression of SOD, GSH, and MDA. In contrast to the administration of baicalein, dexamethasone injection showed similar effects to slow OA progression, while dexamethasone inhibited NLRP3 inflammasome partly through decreasing levels of SOD, GSH, and MDA. This study indicated that baicalein may have the potential for OA prevention and exerts anti-inflammatory effects partly via suppressing NLRP3 inflammasome activation without affecting oxidative stress-associated molecules, and inhibition of cartilage catabolism enzymes in an OA rat model.

Purpose To determine an optimal embargo period preceding release of radiologic test results to an online patient portal. Materials and Methods This prospective discrete choice conjoint survey with modified orthogonal design was administered to patients by trained interviewers at four outpatient sites and two institutions from December 2016 to February 2018. Three preferences for receiving imaging results associated with a possible or known cancer diagnosis were evaluated: delay in receipt of results (1, 3, or 14 days), method of receipt (online portal, physician's office, or phone), and condition of receipt (before, at the same time as, or after health care provider). Preferences (hereafter, referred to as utilities) were derived from parameter estimates (β) of multinomial regression stratified according to study participant and choice set. Results Among 464 screened participants, the response and completion rates were 90.5% (420 of 464) and 99.5% (418 of 420), respectively. Participants preferred faster receipt of results (P.001) from their physician (P.001) over the telephone (P.001). Each day of delay decreased preference by 13 percentage points. Participants preferred immediate receipt of results through an online portal (utility, -.57) if made to wait more than 6 days to get results in the office and more than 11 days to get results by telephone. Compared with receiving results in their physician's office on day 7 (utility, -.60), participants preferred immediate release through the online portal without physician involvement if followed by a telephone call within 6 days (utility, -0.49) or an office visit within 2 days (utility, -.53). Older participants preferred physician-directed communication (P.001). Conclusion The optimal embargo period preceding release of results through an online portal depends on the timing of traditional telephone- and office-based styles of communication. © RSNA, 2018 Online supplemental material is available for this article. See also the editorial by Arenson et al in this issue.

Background Psoriasis confers elevated risk of coronary-artery disease. Objective Do patients with severe psoriasis have larger epicardial adipose tissue volumes (EAT-V) that are associated with cardiovascular risk? Methods For this cross-sectional study, we recruited dermatology patients with severe psoriasis and control patients without psoriasis or rheumatologic disease themselves or in a first-degree relative. Participants, age 34-55 years without known coronary-artery disease or diabetes mellitus, underwent computed tomography (CT); EAT-V was obtained from non-contrast-CT heart images. Results Twenty-five patients with psoriasis (14 men, 11 women) and 16 controls (5 men, 11 women) participated. Groups had no statistical difference in age; body-mass index; various cardiovascular risk factors (except hs-CRP in men); CT-determined coronary-artery calcium scores or plaque; or family history of premature cardiovascular disease. Mean EAT-V was greater in the psoriasis group compared to controls (P=.04). There was no statistical difference among women; however, male patients with psoriasis had significantly more EAT-V than controls (P=.03), even when corrected for elevated hs-CRP (P=.05). Limitations A single-center convenience sample may not be representative. Conclusions Males with psoriasis without known coronary disease or diabetes had greater EAT-V than controls. EAT-V may be an early identifier of those at increased risk for cardiovascular events. (J Am Acad Dermatol 2021;XX:xxx-xxx)

Massive production of efficient, durable, and low-cost electrocatalysts toward oxygen reduction reaction (ORR) is urgently desired for the development of energy storage and conversion devices. In this study, a facile and cost-effective strategy is proposed for the scalable synthesis of atomically dispersed Fe N C derived from petroleum asphalt (Fe N C@PA) as a reinforced catalyst for ORR. The Fe N C@PA is fabricated through a layer-by-layer cladding template and subsequent pyrolysis method. Intercalating appropriate amount of petroleum asphalt not only improves the graphitic degree to reinforce the atomic Fe−Nx active sites, but also increases mass yield of the catalyst (~220%) compared with the Fe N C counterpart. Serving as an ORR electrocatalyst, the optimized Fe N C@PA-1:4 provides almost a four-electron transfer pathway (3.96) and exhibits superior electrocatalytic activity with a half-wave potential (E1/2) of 0.90 V to the commercial Pt/C catalyst (E1/2 = 0.86 V), as well as promoted durability and methanol tolerance in alkaline medium. Moreover, the zinc-air battery based on Fe N C@PA-1:4 cathode delivers a high power density of 166.7 mW cm−2. This work may help the massive production of robust atomically dispersed non-noble metal catalysts for ORR and provide a new avenue for the high value-added utilization of petroleum asphalt.

BackgroundLameness caused by osteoarthritis (OA) is one of the main causes of disability in elderly dogs. Non-steroidal anti-inflammatory drugs (NSAIDs) are important tools in the treatment of canine OA. In recent years, due to the many side effects of NSAIDs, patients cannot tolerate or do not want to take the risk of NSAIDs. People are becoming more and more interested in new treatments for canine OA, and so-called nutritional supplements have emerged. Puerarin has a wide range of pharmacological activities and is often used as a clinical prescription drug and dietary supplement in China. However, the effect of puerarin on canine OA has not been evaluated. Therefore, the purpose of this study is to evaluate the anti-inflammatory and anti-cartilage degradation effects of puerarin in a canine OA model induced by anterior cruciate ligament transection (ACLT), and to detect the serum inflammatory factor interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) levels and cartilage degradation biomarker C-terminal telopeptides of collagen type II (CTX-II), cartilage oligomeric matrix protein (COMP) and chondroitin sulfate 846 epitope (CS 846) levels in serum and synovial fluid at different periods of puerarin administration. ResultsEight weeks after the administration, the veterinarian performed clinical and imaging evaluations to comprehensively evaluate the protective effect of puerarin on canine OA. Daily oral administration of 20 mg/kg puerarin can significantly inhibit the expression of IL-1β, IL-6 and TNF-α in serum within 8 weeks (P < 0.05), and its anti-inflammatory effect is similar to oral celecoxib (negative control group). Puerarin has a certain protective effect on articular cartilage and can reduce the level of biomarkers CTX-II, COMP and CS 846 in serum and synovial fluid in the early stage of OA (P < 0.05). In addition, the clinical scores and radiographs scores were significantly reduced after 8 weeks of puerarin treatment (P < 0.05). ConclusionsCanine OA cartilage may be mediated through anti-inflammatory, anti-metabolism and anabolic effects, and strongly down-regulate the inflammatory factors IL-1β, IL-6 and TNF-α and cartilage degradation biomarkers CTX-II, COMP and CS 846 are related, providing a good alternative therapy for OA.

Osteoarthritis (OA) is a common joint disease and the main cause of disability. We sought to determine the effective concentration of emodin on chondrocytes and to identify the dosage of emodin that induces a comparable therapeutic effect with the COX-2 inhibitor drug, celecoxib that is currently used to treat OA.In vitro experiments induced inflammation of chondrocytes by IL-1β, and an osteoarthritis model was established in vivo by cutting rat anterior cruciate ligament. Western Blot, Real-time PCR, HE staining, Safranin O-green staining and immunohistochemistry were performed to detect MMP-3, MMP-13, ADAMTS-4, iNOS and COL2A1 on the chondrocytes or the tibial plateau. The cytokine activity and content in serum of six groups of rats were measured by kit.It was found that the surface layer of the cartilage was thicker and smoother after the administration of emodin. Tissue expression of MMP-3, MMP-13, ADAMTS-4 and iNOS were significantly (p 0.05) decreased in chondrocytes and cartilage treated with different doses of emodin, and the content of COL2A1 was reversed. Emodin also significantly decreased the blood levels of COX-2 and PGE2. The effective emodin in vitro was 5 μmol/L, whereas emodin at 80 mg/kg was equivalent to celecoxib in vivo.Emodin reduces the expression of cartilage matrix degradation biomarkers, thereby reducing the degradation of cartilage matrix and protecting the knee joint cartilage. Emodin at 5 μmol/L shows the best concentration to treat chondrocytes, and the protective effect of emodin at 80 mg/kg is comparable to that of celecoxib.

Background This article aims to study the changes of CTX-II and C2C biomarker concentrations during the pathogenesis of osteoarthritis with SD rats as the research object. Through the longitudinal and joint detection of the content of CTX-II and C2C markers in the serum of anterior cruciate ligament resection (ACLT) rats, the evaluation and early diagnosis of OA disease can be realized, and the theoretical basis for the rapid diagnosis technology of OA can be provided. Methods SD rats were randomly divided into two groups: Sham operation group and OA model group. The OA model was established by anterior cruciate ligament excision (ACLT) for 2, 4, 6, 8, and 10 weeks, respectively. The cartilage gross score and Mankin score were used to evaluate the model. The tibia of the right hind limb was sampled for pathological histology and HE staining. The collected blood samples are used to detect changes in the concentration of CTX-II and C2C in serum. The receiver operating characteristic curve (ROC) was used to compare the area under the curve (AUC) of CTX-II, C2C and combined biomarkers. Results In the model group, the content of CTX-II and C2C in SD rat serum increased significantly, and the content of CTX-II and C2C increased with the prolonged modeling time, which was time dependent; The levels of CTX-II and C2C in the serum of rats in the sham operation group did not change significantly; both macroscopic observations and Mankin scores increased significantly. The AUC of the combined biomarker is higher than that of CTX-II and C2C. Finally, CTX-II and C2C levels were positively correlated with Mankin score. Conclusion Early combined detection of serum CTX-II and C2C concentrations has potential value for the evaluation and diagnosis of osteoarthritis.

CF101 (IB-MECA) is an adenosine A3 receptor agonist that has anti-inflammatory and pain-relieving properties. Adenosine A3 receptor activation can delay the process of Osteoarthritis(OA) and prevent the occurrence of OA. However, the mechanism of CF101 on OA is still unknown. This study aimed to investigate the effect of CF101 on rats induced by anterior cruciate ligament-transection (ACLT) and rat chondrocytes induced by IL-1ß. ACLT-induced OA rats were administered CF101, and autophagy levels were measured to determine whether CF101 had an autophagy-mediated protective effect on articular cartilage. Furthermore, the mechanism by which CF101 protected articular cartilage in IL-1ß-induced chondrocytes mimicking OA was investigated. In rats treated with ACLT, CF101 was able to delay the progression of OA, as well as reduce inflammation and type II collagen degradation factors. In addition, in vitro experiments revealed that CF101 reduced type II collagen degradation factors in OA chondrocytes. In rats treated with ACLT and OA chondrocytes, CF101 enhanced autophagy and increased the ratio of AMP/ATP and AMPK protein levels while decreasing mTOR expression. Treatment of OA chondrocytes with 3-MA prior to treatment with CF101 resulted in inhibition of autophagy factor levels, as well as increased levels of inflammatory factors and type II collagen degradation compared to the CF101 group. These findings demonstrated that CF101 could protect articular cartilage against OA by enhancing the ratio of ATP/AMP and altering the AMPK/mTOR pathway to enhance autophagy and reduce inflammation. In addition, inhibition of autophagy resulted in a reduced CF101 effect.

Background To comprehensively evaluate the diagnostic value of serum cartilage oligomeric matrix protein (COMP) and chondroitin sulfate 846 epitope (CS846) biomarkers in osteoarthritis (OA), longitudinal and combined measurement of serum COMP and CS846 were performed at different stages in the pathological process of OA in a rat model of anterior cruciate ligament transection (ACLT). Methods Sixty male Sprague-Dawley rats were randomly divided into two groups, including a model group (n = 30) and a control group (n = 30). Rat models were established by ACLT surgery, and sham operations were performed on rats in the control group. Prior to surgery and at 2, 4, 6, 8, and 10 weeks after ACLT surgery, serum levels of COMP and CS846 biomarkers were determined using an enzyme-linked immunosorbent assay approach. Five rats per group were euthanized at 2, 4, 6, 8, and 10 weeks after surgery, after which tibial plateau specimens were collected. Macroscopic observation and histological examination were employed for rat tibial plateau. Histological changes in articular cartilage were evaluated according to Osteoarthritis Research Society International (OARSI) scoring criteria. The area under the curve (AUC) of COMP, CS846, and combined biomarkers was compared using receiver operating characteristic (ROC) curve. Results Within 10 weeks after surgery, serum levels of COMP and CS846 in the model group were significantly higher when compared to those in the control group. Moreover, a significant correlation was observed between changes in COMP and CS846 levels. At each time point, macroscopic observations and OARSI scores were significantly increased in the development of OA. The AUC of combined biomarkers was higher compared to that of COMP and CS846 alone. Finally, a positive relationship was found between levels of COMP and CS846 and the OARSI score. Conclusions In this study, we found that combined detection of serum CS846 and COMP levels can be used for diagnosis and monitoring of OA progression.

Our aim was to assess and address the challenges radiology residents face when managing breast imaging emergencies on call and to determine if targeted educational interventions improved resident confidence and knowledge. We created surveys to determine resident comfort level with and knowledge of appropriate management of breast imaging emergencies. We also created structured educational interventions to improve resident confidence and knowledge. The effectiveness of these interventions was assessed with pre- and post-intervention surveys given to the 43 residents at our institution. Thirty-six of the 43 residents at our institution completed both surveys. The results showed that 33 of 36 residents (91.7%) felt an increase in their comfort level after utilizing one or both of the interventions. There was also significant improvement in resident knowledge; the average resident score on the knowledge questions improved from 40 to 68% (p

Introduction: The study aimed to clarify the changes in the concentration of inflammatory mediators, proteases, and cartilage degradation biomarkers in the synovial fluid of joints in an equine osteoarthritis model. Material and Methods: Osteoarthritis was induced in eight Mongolian horses by a sterile intra-articular injection of amphotericin B, which was injected into the left carpal joint in a dose of 2 mL (25 mg/mL). The control group comprised five horses which were injected with an equal dose of sterile physiological saline into the left carpal joint. Synovial fluid was obtained at baseline and every week after injection. Test methods were based on ELISA. Results: In the course of the osteoarthritis, the concentration of biomarkers in joint synovial fluid showed an increasing trend. IL-1, IL-6, MMP-9, MMP-13, ADAMTS-5, CS846, GAG, HA, CTX-II, and COMP concentrations sharply increased before the onset of significant symptoms of lameness, whereas TNF-α, MMP-2, and MMP-3 concentrations rose sharply after the occurrence of such symptoms. Conclusion: The results obtained confirm that the concentrations of IL-1, IL-6, MMP-9, MMP-13, ADAMTS-5, CS846, GAG, HA, CTX-II and COMP increase substantially in equine osteoarthritis, which provides a theoretical basis for the rapid diagnosis of the disease.

In osteoarthritis (OA), activated synoviocytes and articular chondrocytes produce pro-inflammatory cytokines, such as IL-1β, that promote chondrocyte apoptosis and activate the NF-κB signaling pathway to induce catabolic factors. In this study, we examined the anti-inflammatory and anti-apoptotic effect of baicalein on IL-1β signaling and NF-κB-regulated gene products in rat chondrocytes. Rat chondrocytes were pretreated with 10 ng/ml IL-1β for 24 h and then co-treated with 10 ng/ml IL-1β and 50 μM baicalein for 0, 12, 24, 36 and 48h. The expression levels of poly(ADP-ribose) polymerase (PARP), Bcl-2, caspase-3, matrix metalloproteinase (MMP)-9, MMP-3, cyclooxygenase (COX)-2 and SOX-9 were detected by Western blot and quantitative reverse transcription-PCR (qPCR). The effects of baicalein on the translocation and phosphorylation of the NF-κB system were studied by Western blotting and immunofluorescence. Baicalein stimulated the expression of anti-apoptotic genes and reduced the pro-apoptotic and pro-inflammatory gene products in chondrocytes. Baicalein promoted SOX-9 expression in a time-dependent manner in chondrocytes. Baicalein inhibited the NF-κB activation that was induced by IL-1β in a time-dependent manner in chondrocytes. Our results suggest that the anti-inflammatory and anti-apoptotic effects of baicalein are mediated through the inhibition of the translocation of phosphorylated p65 to the nucleus.

PBB12, a long noncoding RNA (lncRNA), has not been reported to be involved in the progression of osteosarcoma to date. According to our research data, it was found that osteosarcoma patients with a high PBB12 level frequently showed increased metastasis. Mechanistic research demonstrated that PBB12 can competitively bind to hsa‑miR‑204‑5p by acting as a microRNA sponge. Furthermore, PBB12 intervenes in the Kruppel‑like factor 4 (KLF4)/hsa‑miR‑204‑5p/activating transcription factor 2 (ATF2) pathway and affects the proliferation and invasion of osteosarcoma cells. High PBB12 expression was founld to lead to the loss of function of the cancer suppressors KLF4 and hsa‑miR‑204‑5p; these effects are the intrinsic reason why osteosarcoma patients with high levels of PBB12 often develop tumor metastases. In vitro functional experimental data showed that in the osteosarcoma cell lines MG63 and SAOS‑2, PBB12 silencing and overexpression significantly increases or reversed the inhibitory effect of KLF4 on the proliferation and invasion of tumor cells, respectively. The involvement of the interaction between PBB12 and the KLF4/hsa‑miR‑204‑5p/ATF2 pathway in osteosarcoma progression was reported for the first time, and these data provide important theoretical support for gene therapy targeting KLF4 and hsa‑miR‑204‑5p. The great significance of this study is that a high or low genetic background level of PBB12 in osteosarcoma patients may serve as an important marker for screening patients for a high risk of tumor metastasis. Furthermore, for osteosarcoma patients with high PBB12 expression, the primary task for all accurate personalized clinical treatment programs may be the determination of how to effectively knock down PBB12 in tumor bodies.

Osteoarthritis is a chronic joint disease which has a serious impact on the health and quality of life of affected humans and animals. As an inhibitor of inducible nitric oxide synthase (iNOS), aminoguanidine (AG) displays anti-inflammatory effects. The purpose of the present study was to investigate the effect of AG on the expression of iNOS and cyclooxygenase-2 (COX-2), and the activity of the NF-κB signaling pathway in rat chondrocytes stimulated by interleukin-1β (IL-1β). The viability of chondrocytes treated with AG (0.3, 1 or 3 mM) alone was determined using a Cell Counting Kit-8 assay. Subsequently, the chondrocytes were treated with either 10 ng/ml IL-1β alone, or co-treated with increasing concentrations of AG (0.3, 1 or 3 mM) and 10 ng/ml IL-1β. The protein levels of COX-2, iNOS, phosphorylated (p)-p65, p65, p-NF-κβ inhibitor α (IκBα), IκBα, p-inhibitor of NF-κβ-β (IKKβ) and IKKβ were evaluated by western blotting. NF-κB translocation was determined by immunofluorescence analysis. Western blotting and reverse transcription-quantitative PCR were used to detect expression levels of relevant proteins/genes. The results suggested that the inhibitory effect of AG on the protein and gene expression levels of iNOS and COX-2 in IL-1β-treated chondrocytes was dose-dependent. In addition, AG decreased the level of phosphorylation of IKKβ, IκBα and NF-κB p65, the degradation of IKKβ, IκBα and p65, and the translocation of NF-κB in IL-1β-stimulated chondrocytes. The most significant inhibitory effect of AG was observed at a concentration of 1 mM. Therefore, the present study suggested that AG may serve as a potential agent to reduce the inflammatory response of chondrocytes stimulated by IL-1β.

Purpose: Hyperglycemia affects FDG uptake in the brain, potentially emulating Alzheimer’s disease in normal individuals. This study investigates global and regional cerebral FDG uptake as a function of plasma glucose in a cohort of patients. Methods: 120 consecutive male patients with FDG PET/CT for initial oncologic staging (July–Dec 2015) were reviewed. Patients with dementia, cerebrovascular accident, structural brain lesion, prior oncology treatment or high metabolic tumor burden (recently shown affecting brain FDG uptake) were excluded. 53 (24 nondiabetic) eligible patients (age 65.7 ± 2.8 mean ± SE) were analyzed with parametric computer software, MIMneuro™. Regional Z-scores were evaluated as a function of plasma glucose and age using multi variable linear mixed effects models with false discovery analysis adjusting for multiple comparisons. If the regression slope was significantly (p

BACKGROUND To evaluate the effectiveness and safety of thermal mineral waters therapy for pain relief, and functional improvement, and quality of life (QoL) in patients with osteoarthritis (OA). METHODS Cochrane Library, Web of science, EMBASE, ClinicalTrials.gov and PubMed were systematically searched for randomized controlled trials. Study inclusion criteria included assessment of the visual analog scale and Western Ontario and McMaster Universities scores and the lequesne index to evaluate the effects of thermal mineral waters on pain relief and functional improvement. Also, studies that used the European quality of life 5-dimension scale and health assessment questionnaire to assess the impact of thermal mineral waters therapy on improving QoL were included. RESULTS Sixteen studies were included. A meta-analysis showed that thermal mineral waters therapy could significantly reduce pain as measured visual analog scale and Western Ontario and McMaster Universities assessments (P

The etiology of osteoarthritis (OA) is multifactorial, with no effective disease-modifying-drugs. L-theanine has been reported to inhibit inflammatory responses in some diseases and this study aimed to investigate the effect of L-theanine on Interleukin-1(IL-1)&beta, stimulated chondrocytes, and in an injury-induced OA rat model. Primary chondrocytes were stimulated by IL-1&beta, (10 ng/mL) for 24 h and then co-cultured with L-theanine for 24 h. The effects of L-theanine on IL-1&beta, stimulated expression of pro-inflammatory cytokines and hydrolytic enzyme were analyzed using Western blotting, quantitative polymerase chain reaction (q-PCR) and enzyme-linked immunosorbent assay (ELISA) kits. An immunofluorescence assay was used to detect nuclear factor kappa B (NF-&kappa, B) phosphorylation. OA was induced by anterior cruciate ligament transection (ACLT) surgery in rats and celecoxib was used as a positive control. OA severity was measured using the Osteoarthritis Research Society International (OARSI) grading system to describe histological changes. The results showed that L-theanine decreased the expression of pro-inflammatory mediators, including cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE-2), inducible nitric oxide synthase (iNOS), and nitric oxide (NO), both in vivo and in vitro. L-theanine treatment inhibited IL-1&beta, induced upregulation of matrix metalloproteinases (MMP)-3 and MMP-13, as well as inhibited NF-&kappa, B p65 activation. In vivo animal model showed that L-theanine administration (200 mg/kg) significantly alleviated OA lesions and decreased OARSI score. Our data indicated that L-theanine decreased inflammatory cytokines and protected extracellular matrix degradation through inhibition of the NF-&kappa, B pathway, and L-theanine may be considered a promising therapeutic strategy in OA prevention.

In this study, nitrogen-doped graphene nanoshells (N-GNS) were developed to support palladium nanoparticles (Pd/N-GNS) as an efficient and recyclable catalyst for the N-allylation reaction. N-GNS was synthesized through a facile hard-template method by using petroleum asphalt, followed by nitrogen doping by thermal annealing with urea, the contents and species of which could be altered by the calcination temperature. Palladium nanoparticles (Pd NPs) with an average diameter of 3.3 nm were homogeneously deposited onto the N-GNS support through a mild solvent-growth approach. The Pd/N-GNS exhibited a superior activity towards the N-allylation reaction, 6-fold higher than that of the pristine graphene nanoshells supporting the palladium catalyst. The Pd/N-GNS could be recycled several times without activity deterioration and metal leaching. The catalytic activity showed a linear correlation relationship with the pyridinic N content. Experimental and theoretical studies reveal strong metal-support interactions between the pyridinic N and palladium species, which can downsize the Pd NPs, modulate the electronic properties, and promote the adsorption of reactant, thereby significantly boosting the catalytic efficiency and stability for the N-allylation process. The present work could help unravel the roles of nitrogen-doped carbon supports and provides a feasible strategy to rationally design superior palladium catalysts for chemical transformations.