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Testicular ischemia-reperfusion injury (TIR) is a urological emergency common among male newborns, children, and adolescents. Testicular injury and its consequences, such as altered hormone production, subfertility, and infertility, are determined by the duration and degree of testicular torsion. Early diagnosis and treatment are crucial to preserving the testes and fertility. Previous studies suggest that reactive oxygen species contribute to the pathogenesis of TIR injury, but the underlying mechanism remains unclear. Several drugs/plants reportedly exhibit antioxidative activities to protect against TIR. This review summarizes current studies on the role of antioxidants in preventing experimental TIR injury and discusses the underlying pathophysiological mechanisms.

Correction to: European Review for Medical and Pharmacological Sciences 2020; 24 (19): 10086-10095-DOI: 10.26355/eurrev_202010_23228-PMID: 33090416, published online 15 October, 2020. After publication, the authors received a comment on PubPeer "The characterization of exosomes in this study is very limited. There is no characterization of ultrastructure (EM) and size. The anti-CD63 immunoblot does not have the typical smeared appearance and is therefore questionable. In addition, the text is full of errors and unscientific expressions". The authors thank the reader for pointing out these criticisms and specify that they re-performed some of the assays and then added the exosomes' ultrastructure with TEM. In addition, they replaced a more typical CD63 band. Spelling errors have also been corrected (in the method's section, 'lysate' was changed to 'lysis'). There are amendements to this paper. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/23228.

Inflammation and fibrosis progress of nucleus pulposus (NP) cells participate in the pathologic changes of intervertebral disc degeneration (IDD). ANGPTL2 is well known for its angiogenesis and proinflammatory properties and transforming growth factor β1 (TGF-β1) is also responsible for tissue fibrosis. However, the role of ANGPTL2 in IDD and whether it is related to TGF-β1 remains unclear. This study aims to explore the relation of TGF-β1 and ANGPTL2 in the degenerative process of NP cells.We isolated NP cells of NP tissues provided from the spine fracture patients. IL-1β was used to induce the NP cells degeneration. To determine the effect of TGF-β1 and ANGPTL2 on NP cell degeneration, we regulated the cellular TGF-β1 and ANGPTL2 expression by Recombinant human protein stimulation and siRNA transfection. Quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot was employed to investigate the expression of TGF-β1, ANGPTL2, IL-6, TNF-α, collagen I, and collagen III.TGF-β1 overexpression aggravated the ANGPTL2, IL-6, TNF-α, collagen I, and collagen III expressions of NP cells that caused by IL-1β, which was rejected by ANGPTL2 gene silencing. Besides, the silencing of TGF-β1 weakened the ANGPTL2 expression. ANGPTL2 overexpression promoted the NP cells inflammation and fibrosis via increasing IL-6, TNF-α, collagen I, and collagen III expression, which was sharpened by a consequent increase of TGF-β1 expression.This study, for the first time, points that TGF-β1 aggravates degenerative NP cells inflammation and fibrosis via the mediation of ANGPTL2.

The aim of this study was to explore the changes in the body state of patients with non-small cell lung cancer (NSCLC), including intestinal flora, serum inflammatory factors, immunity and adiponectin.A total of 18 NSCLC patients (disease group) and 16 healthy people from the Medical Center (control group) were selected as research objects. The levels of immune molecules immunoglobulin A (IgA), IgG and IgM, and inflammatory factors interleukin-2 (IL-2), C-reactive protein (CRP), tumor necrosis factor-α (TNF-α) and IL-6 were detected via enzyme-linked immunosorbent assay (ELISA). The level of adiponectin was determined using the quantitative kit. In addition, the changes in intestinal flora were analyzed.The overall survival time of NSCLC patients was significantly affected by IL-2 (p=0.0026), CRP (p=0.03), TNF-α (p=0.014) and IL-6 (p=0.00018). It can be seen that these inflammatory factors may play important roles in the progression of NSCLC. The levels of TNF-α (p=0.037), IL-2 (p=0.043) and CRP (p=0.000) in the peripheral blood serum were significantly higher in disease group than control group. Meanwhile, the levels of IgA (p=0.040) and IgG (p=0.000) in the peripheral blood serum were significantly higher in disease group than control group. However, no significant difference was observed in the level of IgM between the two groups (p0.05). The expression of adiponectin gene (ADIPOQ) could remarkably affect the overall survival rate of NSCLC patients, and patients with high expression of ADIPOQ exerted significantly better prognosis (p=0.017). The level of serum adiponectin was evidently higher in control group than that in disease group (p0.05). According to the linear discriminant analysis (LDA) score of the intestinal flora in both groups, the abundance of some intestinal flora (Enterobacter and Lachnospiraceae) was markedly higher in disease group than control group (p0.05). However, the abundance of Bifidobacteria, Pediococcus and Lactobacillus was remarkably higher in control group than disease group (p0.05). Correlation analysis indicated that Lactobacillus was positively correlated with Bifidobacteria (r=0.44, p=0.000), whereas was negatively correlated with Enterobacter (r=-0.22, p=0.024). Furthermore, Enterobacter was negatively associated with Bifidobacteria (r=-0.15, p=0.038) and Streptococcus (r=-0.12, p=0.046).Serum inflammatory factors, adiponectin, intestinal flora and immunity may play important roles in the development of NSCLC.

To investigate whether human umbilical cord mesenchymal stem cells (UMSCs) derived exosomes (exosome) can repair the heart after myocardial infarction (MI) by delivering circ-0001273 and its mechanism.Through the Sprague Dawley (SD) rat MI model was established, at the same time, we designed si-circ-0001273. Phosphate-buffered saline (PBS), exosome and si-circ-0001273-exosome were transplanted into ischemic hearts of rat, respectively. Through the echocardiography, hematoxylin-eosin staining (HE) method to detect the rat heart recovery. Meanwhile, H9c2 was treated with hypoxic serum-free serum to construct an in vitro apoptosis model to further explore the effect of circ-0001273 on myocardial cell apoptosis.Compared with the exosome-treated group, the left ventricular ejection fraction (EF) and shortened fraction (FS) of the rat heart was remarkably reduced and the cardiac structure was more disordered in the si-circ-0001273-exosome-treated group. Meanwhile, in vitro TUNEL staining and flow cytometry detection, results showed that compared with the exosome co-culture group, the incidence of H9C2 cell apoptosis in the si-circ-0001273-exosome co-culture group was obviously increased.Circ-0001273 can remarkably inhibit the occurrence of myocardial cell apoptosis in ischemic environment, promote MI repair, and provide a good reference for clinical treatment.

In 2016 WHO classification, EBV +DLBCL of the elderly was replaced by EBV+ DLBCL NOS. This is due to the fact that many young patients of EBV+ DLBCL were found in recent years.In this study, we retrospectively analyzed clinical features and survival outcomes of EBV positive DLBCL patients in different age groups. All the patients treated at a single center.When we use different ages (40, 50 and 60 years old) as cutoffs, the prevalence of EBV positive DLBCL was 12.0%, 12.3% and 13.0% in younger patients and 19.0%, 15.4% and 13.8% in elder patients respectively. Whatever the age cutoff was, EBV positive associated with unfavorable clinical prognosis in elder groups. When we use 40 and 50 years old as age cutoffs, poor impacts of EBV positive on overall survival and progression-free survival were observed only in elder patients, but not in younger patients. It should be noted that when we use 60 years old as age cutoff, the results were the opposite.EBV+ DLBCL patients with age of 40 to 60 years old showed poorer prognostic features than EBV- DLBCL patients; however, patients in other age groups did not show evident differences in prognosis between EBV+ DLBCL patients and EBV- DLBCL patients. This finding was not reported before.

The aim of this study was to explore the effect of micro ribonucleic acid (miR)-126 on the apoptosis of retinal ganglion cells in glaucoma rats via the vascular endothelial growth factor (VEGF)-Notch signaling pathway.A total of 36 Sprague-Dawley (SD) rats were randomly divided into three groups, including normal group (n=12), model group (n=12) and miR-126 antagomir group (n=12). Rats in normal group did not receive any treatment. In model group and miR-126 antagomir group, the rats were used to establish glaucoma models and intervened with normal saline and miR-126 antagomir, respectively. Intraocular pressure was detected at the completion of modeling and the last intervention, at 7 days after which samples were taken. Western blotting was adopted to detect the relative protein expressions of Notch1 and Notch2. The content of VEGF was examined via enzyme-linked immunosorbent assay (ELISA). Quantitative polymerase chain reaction (qPCR) was carried out to detect the messenger RNA (mRNA) expressions of VEGF, Notch1 and Notch2. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay was performed to detect cell apoptosis.After modeling, intraocular pressure in model group and miR-126 antagomir group was significantly higher than that in normal group (p0.05). At the end of the intervention, intraocular pressure in miR-126 antagomir group was notably lower than that in model group (p0.05). VEGF content in model group and miR-126 antagomir group was notably higher than that in normal group (p0.05). However, it was markedly lower in miR-126 antagomir group than model group (p0.05). Model group exhibited remarkably higher protein expressions of Notch1 and Notch2 than normal group (p0.05). However, the protein expressions of Notch1 and Notch2 in miR-126 antagomir group were evidently reduced (p0.05). Besides, the mRNA expressions of VEGF, Notch1 and Notch2 in model group were significantly higher than those in normal group (p0.05). However, they were significantly lower in miR-126 antagomir group than those in model group (p0.05). Furthermore, the apoptosis rate in model group was distinctly higher than that in normal group (p0.05). However, it was notably lower in miR-126 antagomir group than model group (p0.05).MiR-126 facilitates the apoptosis of retinal ganglion cells in glaucoma rats by promoting the VEGF-Notch signaling pathway.

The aim of this study was to investigate the effect of leptin (Lep) on the proliferation, invasion and apoptosis of prostate cancer cells through the extracellular regulated protein kinase 1/2 (ERK1/2) signaling pathway.Prostate cancer DU145 cells in the logarithmic growth phase were randomly divided into Lep (10, 20, 40, 80, 160 and 320 ng/mL) groups and blank control (Con) group. After culture, the cells were treated for 6 h, 12 h and 24 h, respectively. The effects of Lep on the proliferation and invasion of DU145 cells were detected via methyl thiazolyl tetrazolium (MTT) assay and transwell chamber assay, respectively. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was carried out to examine the messenger ribonucleic acid (mRNA) expressions of ERK1/2, b-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax) in DU145 cells after Lep treatment for 24 h. Thereafter, immunofluorescence assay was performed to detect the localization of ERK1/2 protein in prostate cancer DU145 cells. In addition, the expressions of phosphorylated (p)-ERK, ERK1/2 and apoptosis-related proteins, Bcl-2, Bax and cleaved cysteinyl aspartate specific proteinase (c-Caspase 3) in prostate cancer DU145 cells after treatment with different concentrations of Lep for 24 h were examined by Western blotting.MTT assay results showed that the proliferation rate of DU145 cells increased significantly at 6 h, 12 h and 24 h after 5-320 ng/mL of Lep treatment (p0.05). Transwell assay manifested that the number of invasive cells was significantly raised after Lep treatment for 24 h (p0.05). Meanwhile, the invasion ability of cells increased gradually with the elevation of Lep concentration. Subsequent qRT-PCR results demonstrated that after treatment with different concentrations of Lep, the mRNA expressions of ERK1/2 and Bcl-2 rose markedly (p0.05). However, the mRNA expression of Bax was remarkably down-regulated (p0.05) with the increase of Lep concentration in a concentration-dependent manner. According to the detection using a laser scanning confocal microscope, ERK1/2 red fluorescence showed punctiform aggregation, which was gradually raised with the increase of Lep concentration for 24 h. Moreover, Western blotting results denoted that with the increase of Lep concentration, the protein expressions of p-ERK, ERK1/2 and Bcl-2 were notably elevated (p0.05), while those of Bax and c-Caspase 3 were distinctly reduced (p0.05).Lep activation induces the proliferation, promotes the invasion and inhibits the apoptosis of prostate cancer cells through the ERK1/2 signaling pathway.

The aim of this study was to explore the effect of micro ribonucleic acid (miR)-200c on the proliferation and apoptosis of Wilms tumor cells, and to further elucidate its potential mechanisms.Reverse Transcription-Polymerase Chain Reaction (RT-PCR) was used to detect the expression level of miR-200c in cancer tissues and adjacent normal tissues of 20 patients with Wilms tumor. Human primary Wilms tumor cells were taken as research objects, and were divided into Control group and miR-200c mimic group. In miR-200c mimic group, miR-200c was overexpressed in Wilms tumor cells using liposome transfection technology. Subsequently, the proliferation and apoptosis of cells in each group were observed by functional assays. The expression levels of phosphorylated protein kinase B (p-Akt), total Akt (T-Akt) and glucose transporter protein type 1 (GLUT1) in each group of cells were finally detected by Western blotting.In Wilms tumor patients, the expression level of miR-200c in cancer tissues was notably lower than that in adjacent normal tissues (p0.05). Wilms tumor cells were cultured in vitro, and were transfected with miR-200c mimic. Subsequent cell counting kit-8 (CCK-8) assay results showed that the proliferation ability of cells in miR-200c mimic group was remarkably weakened (p0.05). Colony formation assay indicated the number of formed colonies in miR-200c mimic group was remarkably less than that in Control group (p0.05). Western blotting results manifested that overexpression of miR-200c markedly increased the ratio of B-cell lymphoma protein 2 (Bcl-2) to Bcl-2-associated X protein (Bax) (p0.05). Flow cytometry results revealed that miR-200c overexpression significantly elevated the apoptosis rate of Wilms tumor cells (p0.05). In addition, it was discovered that the overexpression of miR-200c could prominently reduce the phosphorylation level of intracellular Akt and the expression of its downstream protein GLUT1. Finally, immunohistochemical staining results verified that the expression levels of p-Akt and GLUT1 in cancer tissues of Wilms tumor patients were significantly higher than those in adjacent normal tissues (p0.05).MiR-200c was lowly expressed in cancer tissues of Wilms tumor patients. Besides, overexpression of miR-200c inhibited the proliferation and promoted the apoptosis of cells through targeted inhibition of the Akt/GLUT1 signaling pathway.

We aimed at studying the correlation between TGIF2 expression and clinicopathological features of cervical cancer (CCa). The relationship between TGIF2 and FCMR and its influence on the proliferation and metastasis of tumor cells were investigated using molecular biology techniques, so as to reveal the pathogenesis of CCa and provide a new target for clinical treatment.TGIF2 expression in 60 pairs of cervical tumors and paracancerous tissues samples collected from CCa patients of our hospital was studied by quantitative real-time polymerase chain reaction (qPCR) analysis, and the association between TGIF2 expression and the clinical indicators or prognosis of CCa patients were analyzed. CCa cells with TGIF2 knockdown were constructed using transfection technology. Changes in the biological phenotypes (proliferation, migration, invasion) of CCa cells C33-A and HeLa after TGIF2 knockdown were determined by Cell Counting Kit-8 (CCK-8) and transwell assays. In addition, the effects of TGIF2/FCMR axis on CCa metastasis were further explored in nude mice in vivo.Our data revealed a significant increase in TGIF2 mRNA expression in CCa tissue specimens compared to adjacent ones, and the increasing degree was positively correlated with the incidence of lymph node or distant metastasis of CCa patients. The results of CCK-8 and transwell suggested that knocking down TGIF2 effectively attenuated the proliferative ability and invasiveness of CCa cells. Luciferase assay confirmed that TGIF2 can directly bind to the DNA promoter of its target gene FCMR. Simultaneous transfection of sh-TGIF2 and sh-FCMR partially reversed the inhibitory effect of single transfection of TGIF2 knockdown on the malignant progression of CCa. Experiments in nude mice also suggested that TGIF2 could promote CCa tumorigenesis through the modulation of FCMR expression.In summary, TGIF2 can promote the migration and proliferation ability of cervical cancer cells via down-regulating FCMR. Our study provides a new therapeutic target for the clinical treatment of cervical cancer.

To study the effect of strontium ranelate (SR) on steroid-induced osteonecrosis of the femoral head (SIONFH) in rabbits and its regulatory mechanism.The ONFH model was established in 30 rabbits using steroid and they were randomly divided into Control group, Model group, and SR group. After SR intervention, the rabbits were sacrificed and sampled. The pathological injury of the femoral head in each group was detected via hematoxylin-eosin (HE) staining, the level of vascular endothelial growth factor (VEGF) in the femoral head in each group was detected via enzyme-linked immunosorbent assay (ELISA). The messenger ribonucleic acid (mRNA) and protein expression levels of transforming growth factor-β1 (TGF-β1), as well as the bone morphogenetic protein 2 (BMP2) in the femoral head in each group, were determined using Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western blotting.The rabbit model of SIONFH was successfully established. Compared with Control group, the Model group had a severer pathological injury of the femoral head, a lower level of VEGF in the femoral head, significantly decreased mRNA and protein levels of TGF-β1 and BMP2. Compared with Model group, the SR group had markedly improved pathological injury of the femoral head, a higher level of VEGF in the femoral head, significantly increased mRNA and protein levels of TGF-β1, as well as BMP2.SR can remarkably improve the pathological injury of the femoral head and increase the expression of VEGF in SIONFH rabbits, whose potential mechanism may be related to the activation of the TGF-β1/BMP2 signaling pathway.

Massage therapy is one of the most widely accepted alternative form of medicine helping patients suffering from varied pathological states including arthritis, anxiety, sleep problems, pain management and injury repair. Besides this, it is one of the safest forms of alternative medicine and has become favorite among various health care professionals. However, there is still a lot of debate is going in medical world pertaining to its certain use in modern medicine. So, the present review shall enlighten all the latest aspects of massage therapy in current medicine.

Breast cancer remains a major health problem even with all the recent technological advancements. Large-scale gene expression analysis has offered great ease for both biological characterization and therapeutic planning of breast cancer. Previous studies mostly used variance/regression analysis, which becomes fundamentally flawed when there are unaccounted array specific factors. Here we aim to investigate the underlying mechanism of breast cancer through partial least squares (PLS) based gene expression profile analysis.With a gene expression profile data set downloaded from the Gene Expression Omnibus database, we performed PLS based analysis.We acquire 932 and 771 differentially expressed genes (DEGs) in breast cancer metastasis of estrogen-receptor (ER)-positive and ER-negative patients, respectively. For ER-positive patients, 32 pathways were found to be enriched with DEGs, including immune related pathways, cellular processes and environmental information processing pathways. Survival analysis demonstrated that 18 of them were closely related with non-recurrence rate along time after surgery. For ER negative patients, only three pathways including the folate biosynthesis pathway were enriched with DEGs and none of them overlapped with those of ER positive patients. Only the cholinergic synapse pathway was significantly associated with the non-recurrence rate according to the survival analysis.Our findings shed light on pathways involved in breast cancer relapse with the hope to give some theoretical supports for further therapeutic study.