Search

This document is a corrigendum for an article titled "miR-590-5p may regulate colorectal cancer cell viability and migration by targeting PDCD4." The corrigendum acknowledges that certain data panels in Figure 3 of the original article contained overlapping sections of data, which were assembled incorrectly. The revised version of Figure 3, featuring alternative data from one of the repeated experiments, is provided. The authors state that these errors did not significantly impact the overall results or conclusions of the study. They apologize for any inconvenience caused and express gratitude to the editor for allowing them to publish this corrigendum. [Extracted from the article]

The blood-brain barrier (BBB) is critical for proper cerebral homeostasis and its dysfunction during ischemic stroke can result in significant neurological injury. The major goal of the present study was to identify whether curcumin pretreatment possessed protective effects on BBB integrity during the 24 h of acute ischemic brain injury. To investigate the protective effects of curcumin, male Sprague-Dawley rats were divided into multiple groups, including sham, middle cerebral artery occlusion/reperfusion (MCAO/R) vehicle and curcumin pretreated MCAO/R groups. The effects of curcumin were measured by analyzing neurological deficits, infarct size, BBB permeability and expression levels of permeability-related proteins in the brain. It was found that curcumin pretreatment significantly improved neurological scores, decreased infarct size, and protected synaptic remodeling of hippocampal neurons and upregulated the protein expression level of tight junction proteins, ZO-1, occludin and claudin-5 in ischemic rat brains. Furthermore, curcumin pretreatment before stroke was shown to downregulate the phosphorylation of NF-κB and MMP-9, which are central mediators of inflammation. The results from the present study indicated that curcumin pretreatment ameliorated ischemic stroke injury by protecting BBB integrity and synaptic remodeling, as well as inhibiting inflammatory responses. [ABSTRACT FROM AUTHOR]

Recent studies have revealed that microRNAs (miRs) are involved in the pathogenesis of colorectal cancer (CRC); however, the roles of miR-590-5p in CRC are not completely understood. Therefore, the present study investigated the expression of miR-590-5p and programmed cell death 4 (PDCD4) in CRC tissues and healthy adjacent tissues via reverse transcription-quantitative PCR. Furthermore, human CRC cells were cultured in vitro and transfected with miR-590-5p inhibitor. CRC cell viability, migration and invasion were evaluated by conducting MTT, wound healing and Transwell assays, respectively. Additionally, the relative expression of PDCD4 and phosphorylated-Smad2/3 was analyzed via western blotting. miR-590-5p was significantly upregulated and PDCD4 was significantly downregulated in CRC tissues compared with healthy adjacent tissues. Moreover, the results indicated that miR-590-5p knockdown inhibited cell viability and migration by altering the expression of PDCD4, transforming growth factor-β and phosphorylated-Smad2/3. PDCD4 was identified as a direct target of miR-590-5p. In conclusion, the results of the present study suggested that miR-590-5p may regulate CRC cell viability and migration, indicating that miR-590-5p may serve as a potential therapeutic target for CRC. [ABSTRACT FROM AUTHOR]

This study aimed to elucidate the role of long non-coding RNA activated by transforming growth factor-β (lncRNA-ATB) in ovarian cancer and its underlying mechanisms of action. Expression levels of lncRNA-ATB in ovarian cancer cell line SKOV3 and in a healthy human ovarian cell line were compared using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results indicated that lncRNA-ATB was expressed at significantly higher levels in SKOV3 cells compared with the healthy cell line. After downregulation of lncRNA-ATB expression in SKOV3 cells using lncRNA-ATB-short hairpin RNA, cell proliferation, apoptosis, invasion and migration were assessed using Cell counting kit-8, Live Dead staining, Transwell assay and wound healing assay, respectively. RT-qPCR and western blotting were used to quantify the expression of signal transducer and activator of transcription 3 (STAT3), phosphorylated (p)-STAT3, and the additional epithelial to mesenchymal transition (EMT)-related proteins E-cadherin and vimentin in SKOV3 cells. LncRNA-ATB downregulation significantly reduced SKOV3 cell proliferation, invasion and migration, promoted apoptosis, decreased the expression of p-STAT3 and vimentin, and increased E-cadherin expression. Taken together, these results suggest that lncRNA-ATB downregulation can inhibit ovarian cancer cell proliferation, invasion and migration, and promote cell apoptosis. Lnc-RNA-ATB may therefore be a new target for ovarian cancer treatment. [ABSTRACT FROM AUTHOR]

Biomechanical methods may provide a novel way to understand blood accumulation in intracerebral hemorrhage (ICH). The current study presents the results of a biomechanical analysis of blood accumulation in ICH using a finite element analysis, with an emphasis on the pressure exerted by the mass effect of blood in early ICH. A two-dimensional finite model of the human brain parenchyma and the human ventricular system was developed and analyzed under two preloading conditions. The material properties of the human parenchyma were derived from previous reports. Ogden's theory was applied to describe the stress-strain association in soft tissue. The results of the present study indicated that maximal stress was located at the two ends of the hemorrhage cavity, with the majority of stresses distributed on the zone surrounding the bleed. The two load environments demonstrated similar stress distributions. The loads put on the detached edges were not less than the intracranial pressure (ICP) when the stress threshold was reached. The results of the present study suggest that the direction of blood accumulation can be determined by the shape of the initial blood mass. Mechanical factors (blood pressure and ICP) did not serve a definitive role in preventing blood from accumulating in the early stages of ICH. The present study may aid in understanding the effects of mechanical factors in blood accumulation and hemostasis in patients with early ICH. [ABSTRACT FROM AUTHOR]

Intracerebral hemorrhage (ICH) may lead to physical and pathological damage and has been a focus of research for decades. Evaluating tensile damage caused by deformation in ICH is an important component of damage assessment for correct diagnosis and treatment. Traditional research on ICH paid little attention to quantified brain tissue damage resulting from mechanical factors, and only a few reported the mechanical properties of damaged brain tissue. The aim of the present study was to present an effective method that is able to evaluate the tissue damage degree in ICH, based on strain energy function. Two finite element analysis (FEA) models were analyzed: A three-dimensional (3D) model for tissue's tension experiment and a two-dimensional (2D) model for brain tissue's deformation in ICH. The polynomial fitting function of stress vs. stretch curve, which was derived from previous reports, was used in the FEA as the constitutive function of brain tissue. The present study demonstrated that white matter could be regarded as hyperelastic material when stretch was <1.343, and with stretch increasing, tissue injury exacerbated when stretch was >1.343. The strain energy loss was not linear in this process, and Neo-Hookean and Ogden model's results demonstrated a similar change in trend, but a difference in quantity. The results from 2D and 3D simulation, respectively, demonstrated the degree of damage according to the above dividing criteria and the possible distribution of tissue damage after ICH ictus. An analytical model from a biomechanical perspective for white matter injury in ICH may facilitate to improve clinical diagnosis and treatment. [ABSTRACT FROM AUTHOR]

The clinical effect of acupuncture in combination with rehabilitation therapy for post-stroke shoulder-hand syndrome (SHS) was explored. Patients (178) with post-stroke SHS who received treatment in the Dalian Second Hospital from March 2012 to March 2016 were included in this study. The patients were divided into experimental group (89 cases) and control group (89 cases). Patients in the control group received rehabilitation therapy, while those in the treatment group received acupuncture treatment in addition to rehabilitation therapy. Visual analogue scale (VAS) was applied to assess the pain degree of patients. Fugl-Meyer assessment (FMA), functional comprehensive assessment (FCA) and assessment of quality of life (QoL) were used to evaluate rehabilitation condition of the patients. Early pain relief, rehabilitation of upper extremity motor function and improvement of QoL after treatment were compared between the two groups. The scores of VAS, FMA, FCA and QoL showed obvious differences between the two groups after treatment (P<0.05). The scores of the experimental group were significantly better than those of the control group, and the improvement in upper extremity motor function of the patients in the experimental group was better than that of the patients in the control group. The total effective rate of the patients in the experimental group was higher than that of control group (P<0.05). The effect in improving the upper extremity motor function of the patients in the experimental group was better than that of control group. The scores of QoL of the patients in the experimental group were better than that of the patients in the control group (P<0.05). In conclusion, acupuncture in combination with rehabilitation therapy can improve early pain and rehabilitation significantly and enhance QoL for patients with post-stroke SHS, which is worthy of being widely used in clinical practice. [ABSTRACT FROM AUTHOR]

Cerebral ischemic stroke is the primary cause of stroke-associated mortality and disability, and current therapeutic options are limited and ineffective. The present study aimed to investigate the potential of apoptotic therapy and the role of microRNA (miR)-424 in cerebral ischemic stroke. PC12 cells, a cloned cell line from rat adrenal pheochromocytoma, were treated with CoCl2 to construct a cellular ischemia model. mRNA and protein levels of programmed cell death protein 4 (PDCD4), Bcl-2, Bax, caspase-3, PI3K and AKT were evaluated using reverse transcription-quantitative PCR and western blot analyses, respectively. Cell Counting Kit-8 assays were performed to examine cell viability in the ischemia model. Flow cytometry was conducted to evaluate the apoptosis of ischemic cells. Furthermore, a luciferase assay was performed to verify the target gene of miR-424. It was revealed that the expression level of miR-424 was downregulated in the ischemia model, while the expression of PDCD4 was upregulated. Moreover, the expression of miR-424 was increased after treatment with miR-424 mimics. The mRNA and protein expression of PDCD4 was upregulated after transfection with pcDNA3.1-PDCD4. PDCD4 was predicted and demonstrated to be a target of miR-424. Notably, overexpression of miR-424 increased cell viability and inhibited apoptosis in the ischemia model, which was reversed by co-treatment with pcDNA3.1-PDCD4. Furthermore, overexpression of miR-424 regulated the expression of PDCD4, Bax, Bcl-2, phosphorylated-PI3K/AKT and caspase-3, which was restored after co-transfection with pcDNA3.1-PDCD4. Collectively, the results indicated that miR-424 regulated the progression of cerebral ischemic stroke in a cellular model by targeting PDCD4. [ABSTRACT FROM AUTHOR]