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Background Doxorubicin (DOX) is widely used as an effective chemotherapy agent in human cancer. Our study aimed to explore the specific mechanism of DOX in osteoarthritis (OA). Methods A mouse OA model was established by destabilizing the medial meniscus (DMM), and the role of DOX was determined by intraperitoneally injecting 5 or 10 mg/kg DOX. The expression of collagen type-II (Col-2) was detected by immunohistochemistry staining, and the expression of plasma interleukin (IL)-6 (IL-6), IL-1beta (IL-1β), and tumor necrosis factor (TNF)-alpha (TNF-α) was evaluated by specific ELISA kits, and the expression of Sry-related HMG box 9 (SOX-9) was detected by western blot. Bone marrow mesenchymal stem cells (BMMSCs) were used to explore the mechanism of DOX in vitro. Reactive oxygen species (ROS) production was determined by flow cytometry. Cell viability was measured by Cell Counting Kit-8 (CCK-8) assay. Chondrocyte differentiation was evaluated by Alcian blue staining assay. The expression of chondrocyte differentiation-related markers was detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Results DOX exposure exacerbated OA progression and inhibited chondrocyte differentiation of BMMSCs. DOX also increased ROS production in BMMSCs. Meanwhile, DOX further increased the elevation of plasma IL-6, IL-1β and TNF-α induced by DMM and obviously reduced the expression of chondrocyte differentiation-related markers, including collagen type II a1 (Col2A1), collagen type X alpha 1 (Col10A1), and aggrecan. Moreover, ROS scavengers NAC and MitoQ efficiently alleviated DOX toxicity, including ROS production and chondrocyte differentiation in BMMSCs. Conclusion Our study revealed that DOX suppressed chondrocyte differentiation by stimulating ROS production, providing a novel theoretical strategy for the clinical treatment of OA caused by DOX.

Background: It has been reported that lncRNA CYTOR suppresses LPS-induced inflammation, which plays crucial roles in osteoarthritis (OA). This study was therefore performed to analyze the role of CYTOR in OA.Methods: Expression of CYTOR and miR-10a-5p in OA patients and chondrocytes as well as healthy patients and chondrocytes was determined by RT-qPCR. The interaction between CYTOR and miR-10a-5p was predicted by IntaRNA online program and confirmed by dual luciferase activity assay. The role of CYTOR and miR-10a-5p in regulating the apoptosis of chondrocytes were analyzed by cell apoptosis assay.Results: CYTOR was under-expressed in OA patients and chondrocytes, and miR-10a-5p was overexpressed in OA patients and chondrocytes. After treatment, CYTOR was upregulated and miR-10a-5p was downregulated. CYTOR was predicted to interact with miR-10a-5p, and the interaction between them was confirmed by dual luciferase reporter assay. Overexpression of CYTOR and miR-10a-5p failed to affect the expression of each other. Cell apoptosis analysis showed that CYTOR overexpression reduced the enhancing effects of miR-10a-5p overexpression on the apoptosis of OA chondrocytes. Conclusion: CYTOR may suppress the development of OA by serving as a ceRNA for miR-10a-5p.

Background The pandemic of coronavirus disease 2019 (COVID-19) caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) presents an unprecedented challenge to prevention and treatment. We aim to describe the clinical characteristics and risk factors of COVID-19 patients needing use assisted ventilation therapy. Methods In this retrospective cohort study, we included 288 adult inpatients diagnosed with COVID-19 in Guangzhou Eighth People's Hospital. We extracted and compared characteristics between patients using continuous positive airway pressure (CPAP) or not. A binary logistic regression model was used to identify risk factors associated with using CPAP therapy. Results COVID-19 patients with CPAP therapy were older and had higher levels of white blood cells (WBC), procalcitonin (PCT), C-reactive protein (CRP), alanine aminotransferase (ALT), D-dimer, but had lymphopenia. They were also more prone to appear bilateral pneumonia, develop into severe or critically severe cases, and receive ICU admission. Multivariate regression analysis showed that each 1-year increase in age (OR, 1.04; 95%CI, 1.01-1.08; P = 0.013), respiratory rate over 24 times per min (OR, 4.78; 95%CI, 1.08-13.17; P = 0.037), diarrhea (OR, 9.62; 95%CI, 1.57-18.31; P = 0.011), ALT greater than 50 U/L (OR, 6.59; 95%CI, 1.35-15.89; P = 0.003), WBC greater than 10×10⁹/L (OR, 5.42; 95%CI, 2.04-14.75; P = 0.008), PCT greater than 0.05 ng/mL (OR, 7.22; 95%CI, 1.64-18.51; P = 0.018), and CRP greater than 10 mg/L (OR, 8.58; 95%CI, 2.28-20.36; P = 0.030) were risk factors for COVID-19 inpatients with assisted ventilation. Conclusion The older age, tachypnea, and gastrointestinal infections showing as diarrhea, elevated ALT, and elevated white blood cells, procalcitonin and C-reactive protein were risk factors for COVID-19 inpatients with assisted ventilation. Investigating and monitoring these factors could help clinicians identify patients with poor prognosis at an early stage and take proactive assisted ventilation to benefit patients.

Previous studies on coronavirus disease 2019 (COVID-19) have focused on the general population. However, cardiovascular disease (CVD) is a common comorbidity that has rarely been investigated in detail. This study aims to describe clinical characteristics and determine risk factors for intensive care unit (ICU) admission of COVID-19 patients with CVD. In this retrospective cohort study, we included 288 adult patients with COVID-19 in Guangzhou Eighth People's Hospital from January 15, 2020 to March 10, 2020. Demographic characteristics, laboratory results, radiographic findings, complications, and treatments were recorded and compared between CVD and non-CVD groups. A binary logistic regression model was used to identify risk factors associated with ICU admission for infected patients with underlying CVD. COVID-19 patients in the CVD group were older and had higher levels of troponin I (TnI), C-reactive protein (CRP), and creatinine. They were also more prone to develop into severe or critically severe cases, receive ICU admission, and require respiratory support treatment. Multivariate regression analysis showed that the following were risk factors for ICU admission in COVID-19 patients with CVD: each 1-year increase in age (odds ratio (OR), 1.08; 95% confidence interval (CI), 1.02-1.17; p = 0.018); respiratory rate over 24 times per min (OR, 25.52; 95% CI, 5.48-118.87; p < 0.0001); CRP higher than 10 mg/L (OR, 8.12; 95% CI, 1.63-40.49; p = 0.011); and TnI higher than 0.03 μg/L (OR, 9.14; 95% CI, 2.66-31.43; p < 0.0001). Older age, CRP greater than 10 mg/L, TnI higher than 0.03 μg/L, and respiratory rate over 24 times per minute were associated with increasing odds of ICU admission in COVID-19 patients with CVD. Investigating and monitoring these factors could assist in the risk stratification of COVID-19 patients with CVD at an early stage.

Glomerular filtration rate (GFR) estimation equations using creatinine and Cystatin-C appear to be superior to those based on creatinine or Cystatin-C in older adults. We sought to compare the performances of those based on creatinine and Cystatin-C in Chinese older adults with chronic kidney disease (CKD). A total of 368 Chinese elderly with CKD underwent the dynamic imaging with technetium-99m diethylene-triamine-pentaacetic acid (99mTc-DTPA), and serum creatinine and Cystatin-C were measured on the same day. The comparison of GFR equations which were creatinine and Cystatin-C-based including chronic kidney disease epidemiology collaboration (CKD-EPI) equation (CKD-EPI-Cr-Cys), Berlin Initiative Study (BIS) equation (BIS-Cr-Cys, also known as BIS-2), MA equation (MA-Cr-Cys), and FENG equation (FENG-Cr-Cys) was conducted. Four equations overestimated GFR except for BIS-2 equation in mGFR ≥ 60 ml/min/1.73 m2 (bias: − 1.40, p = 0.7) and CKD-EPI-Cr-Cys equation in mGFR

In the above paper, the authors realize that an error inadvertently appeared in the funding section on p. 895. Where "This study was supported by the National Natural Science Foundation of China Science Fund Project (grant no. 30960389 and 8176010097)" was written, the application number 8176010097 was featured incorrectly: This should have been written as grant no. 81760030. Therefore, this sentence in the funding section should have read as follows: "This study was supported by the National Natural Science Foundation of China Science Fund Project (grant nos. 30960389 and 81760030)". The authors regret this error was not noticed prior to the publication, and apologize to their funding body and to the readership of the Journal for any inconvenience caused. [the original article was published in International Journal of Molecular Medicine 42:883-896, 2018; DOI: 10.3892/ijmm.2018.3682].

The present study aimed to investigate the effect of the expression of interleukin (IL)-18 and related markers on deep venous thrombosis (DVT) to examine their correlation. Sprague-Dawley rats of different models were established and were randomly assigned into three groups. The expression of IL-18, nuclear factor (NF)-κB and von Willebrand factor (vWF) were detected in blood samples. The inferior vena cava (IVC) was ligated to establish the DVT model. Rat IL-18 overexpression and inhibition vectors were constructed. The expression levels of IL-18 and related markers in the venous wall were compared between the model group and the control group using reverse transcription-quantitative polymerase chain reaction and western blot analyses. Following the culture of human umbilical vein endothelial cells (HUVECs), IL-18 was added to the cells, following which the growth of the HUVECs, and changes in vWF and other endothelial functional markers were analyzed. The IVC model demonstrated complete thrombosis at 8 h and stable thrombosis at 24 h. At 24 h following model establishment, the expression levels of IL-18, NF-κB and vWF were high in the blood samples with the occurrence and development of thrombosis (P

Background/Aims: Although dialysis patients have a higher risk of morbidity and mortality related to cardiovascular disease (CVD) than the general population, the mortality and associated risk factors in Asian dialysis patients with CVD have not been well examined. Methods: In this prospective cohort study, mortality and risk factors were investigated in 591 dialysis patients who were recruited from two dialysis centers from May 1, 2009 to May 1, 2014. The Cox proportional hazards regression assessed adjusted differences in mortality risk. A multivariate analysis was also performed, comparing the CVD and non-CVD groups. Results: A total of 591 patients were enrolled in this study (mean age, 52.05 ± 16.46 years [SD]; 61.8% men; 20.8% with CVD), with a median follow-up of 21.9 (maximum, 72) months. The cumulative hazard of mortality was significantly higher in CVD patients (hazard ratio [HR], 1.835; 95% confidence interval [CI], 1.023-3.293; P=0.042) than in their non-CVD counterparts after adjusting for various confounders. On multivariate Cox analysis, stroke (HR, 4.574; 95% CI, 2.149-9.736; PConclusion: All-cause mortality was significantly higher in the CVD group than in the non-CVD group. Stroke is an independent risk factor for all-cause mortality in dialysis patients with CVD. These findings warrant further studies into preventive and interventional strategies.

It is unclear whether green fluorescent protein (GFP) expression is maintained during the course of multilineage differentiation of muscle-derived stem cells (MDSCs). We isolated MDSCs from GFP-transgenic mice and transferred them to chondrogenic, neurogenic or myogenic media. Multilineage differentiation was examined by morphological observation, histological staining, immunocytochemical staining, real-time RT-PCR and Western blot. Both differentiated cells and non-differentiated cells maintained stable GFP expression until the cells exhibited a senescent phenotype. Thus, MDSCs from GFP-transgenic mice have multilineage potential in vitro and that GFP expression does not influence the multilineage potential of MDSCs (or vice versa).

Purpose This study was a retrospective analysis of early and mid-term clinical effects and perioperative management of cementless bilateral synchronous total hip arthroplasty (THA) in patients with ankylosing spondylitis (AS) with bilateral hip ankylosis. Methods Fifteen AS patients (30 hips) with bilateral hip ankylosis were managed with cementless bilateral synchronous THA. Surgical outcome was evaluated using the visual analogue scale (VAS), the range of motion and the Harris score. Results The mean follow-up period was 29.3 months. At the last follow-up visit, the VAS score decreased from 7.53±0.99 before the operation to 2.40±0.91. The Harris score increased from 24.8±7.42 before the operation to 83.8±4.61. The total range of motion increased from 78.73±14.53 before the operation to 209.73±16.19 after the operation. After the operation, there was one case of early hip dislocation, one case of femoral nerve stretch injury and one case of superficial incision infection. There were no cases of deep venous thrombosis. X-ray examinations did not show prosthetic loosening or displacement. Conclusion AS patients with bilateral hip ankylosis can be treated with cementless bilateral synchronous THA, which could greatly improve hip joint function without significant complications. The clinical effects proved to be satisfactory.

In order to find new drugs to inhibit nitric oxide (NO) production, the effects of pyrrolidine dithiocarbamate (PDTC), a nuclear factor-kappa B (NF-kappaB) inhibitor, on recombinant human interleukin-1beta (rhIL-1beta)-induced NO production in chondrocytes were investigated. Rat chondrocytes were isolated and cultured, divided into control, P0, P1, P2, P3 and P4 groups. The chondrocytes in the P0, P1, P2, P3 and P4 groups were treated with different concentrations of PDTC (0, 3, 10, 30, and 50 micromol/L respectively) for 1 h and then incubated with 5 U/mL rhIL-1beta for 24 h. NO assay kit and RT-PCR were used to detect the NO content and the iNOS mRNA expression in the chondrocytes. The expression level of iNOS mRNA in control, P0, P1, P2, P3 and P4 groups was 0.02+/-0.01, 1.24+/-0.13, 1.21+/-0.14, 0.61+/-0.11, 0.40+/-0.09, 0.21+/-0.06, and the relative content of NO was 15.8+/-2.7, 100+/-14.8, 92.6+/-9.3, 68.3+/-14.2, 27.5+/-9.8, 19.8+/-3.6, respectively. In the P0, P1, P2, P3 and P4 groups, the expression of iNOS mRNA and NO production were significantly increased as compared with those in the control group. As compared with the P0 group, the expression of iNOS mRNA and NO content in control group were lower. In the P2, P3 and P4 groups, PDTC could significantly inhibit the expression of iNOS and NO production induced by rhIL-1beta in a concentration-dependent manner. It is suggested that PDTC can inhibit NO production and iNOS mRNA expression induced by IL-1beta, which may provide an alternative method for the treatment of osteoarthritis.