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Renal ischemia/reperfusion injury (RIRI) represents the principal factor underlying acute kidney injury (AKI), which primarily stems from cellular injuries and ferroptosis caused by reactive oxygen species (ROS). Salidroside (SA), an antioxidant natural ester, has been attributed with the potential to protect against RIRI. In the present study, rats received daily SA doses (1, 10, or 100 mg/kg) by gavage for 7 consecutive days before surgery. The results revealed aggravated renal injury in the RIRI group, which was effectively prevented by SA pretreatment (10 and 100 mg/kg), with the 1 mg/kg dosage demonstrating lesser efficacy. Additionally, the results indicated that SA pretreatment mitigated the RIRI-related upregulation of antioxidative superoxide dismutase. In vitro studies corroborated SA's ability to maintain hypoxia/reoxygenation-treated NRK cell viability, with the protective effect being observed at SA concentrations ≥1 µM and peaking at 100 µM. Furthermore, the results showed that SA safeguarded renal tubular epithelial cells from oxidative damage, reduced ROS accumulation, and inhibited ferroptosis via activation of the PI3K/AKT signaling pathway. Therefore, the results of the present study highlight the promising therapeutic potential of SA as an effective intervention for RIRI via targeting of PI3K/AKT signaling pathway-mediated anti-oxidative and anti-ferroptotic mechanisms. [ABSTRACT FROM AUTHOR]

The present study investigated the protective effects and molecular mechanism of prostaglandin A1 (PGA1) and triptolide (TRI) on apoptosis of cardiac microvascular endothelial cells (CMVECs) in rats. CMVECs of rats were isolated and then cultured. MTT method was used to select and establish a cell hypoxia reoxygenation cell model. The cells were divided into four groups: Normoxia control group (C, normal oxygen), hypoxia reoxygenation group (H/R, hypoxia for 12 h/reoxygenation for 6 h), PGA1 group (H/R+PGA1) and TRI group (H/R+TRI). The growth of cells in each of the group was observed. B-cell lymphoma 2 (Bcl-2) mRNA expression in CMVECs and expression of Bcl-2 mRNA after PGA1 and TRI treatment were determined by RT-PCR. Cell apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay. Bcl-2 mRNA decreased significantly after hypoxia stimulation of CMVECs of rats. The expression of Bcl-2 mRNA was significantly higher in comparison to hypoxia stimulation group after treatment with PGA1 and TRI (P<0.01). The elevated effect of PGA1 on Bcl-2 mRNA was stronger than that of the TRI group (P<0.05). The number of CMVECs reduced significantly after hypoxia. By contrast, DNA fragmentation and the number of endothelial cell apoptosis were increased significantly. However, Bcl-2 mRNA expression decreased significantly, after PGA1 and TRI treatments. Furthermore, the number of apoptotic cells reduced and Bcl-2 mRNA expression increased (P<0.01). PGA1 and TRI significantly upregulated the expression of Bcl-2 mRNA, inhibited the activation of CMVECs and were able to achieve the protective effect on apoptosis of CMVECs in hypoxia.oxygenated rats. [ABSTRACT FROM AUTHOR]

The aim of the current study was to evaluate the use of two-dimensional strain echocardiography (2DS) in quantifying right ventricular (RV) function in patients with pulmonary arterial hypertension (PAH). A total of 41 patients with PAH and 40 healthy control patients were recruited to the study. 2DS was used to determine the strain (ε) and strain rate (SR) of basal, middle and apical segments of the RV free wall. The aforementioned indicators were compared with measurements of RV function taken by conventional ultrasound and right heart catheterization. The ε and SR of all segments of the right ventricular free wall were significantly lower in the PAH group, as compared with the control group (P<0.05). In the PAH group, the ε and SR of the middle and apical segments were significantly lower compared with basal segments (P<0.01). The SR of the apical segments were positively correlated with the area and diameter of the right ventricular. The ε of the apical segments were positively correlated with RV area, diameter and systolic function. The ε and SR of apical segments were positively correlated with pulmonary artery pressure and pulmonary vascular resistance measured by right heart catheterization. These findings indicated that 2DS can accurately evaluate RV longitudinal systolic function. [ABSTRACT FROM AUTHOR]

Gastric cancer is one of the most common types of human cancer associated with a poor prognosis. MicroRNAs (miRs), a class of non-coding RNAs that are 18-25 nucleotides in length, act as key regulators in gene expression, and have been implicated in various human cancer types. miR-125b has been implicated in the malignant progression of gastric cancer. However, the association between miR-125b expression, clinicopathological characteristics and trastuzumab resistance in human epidermal growth factor receptor 2 (HER2)-positive gastric cancer remains unclear. In the current study, in situ hybridization data demonstrated that 81.8% (108/132) of gastric cancer tissues exhibited positive expression of miR-125b, while only 26.3% (10/38) of non-tumor gastric tissues were miR-125b-positive. Reverse transcription-quantitative polymerase chain reaction data indicated that the expression level of miR-125b was markedly increased in gastric cancer tissues compared with non-cancerous gastric tissues. Furthermore, the miR-125b level was significantly associated with tumor (T) stage, lymph node metastasis, distant metastasis and TNM stage of gastric cancer (P<0.05). Increased miR-125b expression predicated poor prognosis in patients with gastric cancer. For HER2-positive gastric cancer, the upregulation of miR-125b expression was significantly associated with advanced malignant progression, as well as a poor prognosis (P<0.05). Furthermore, data from the present study indicated that the increased miR-125b level was significantly associated with trastuzumab resistance in HER2-positive gastric cancer (P<0.05). Therefore, the current study suggests that miR-125b may become a potential biomarker for predicting prognoses and clinical outcomes in patients with HER2-positive gastric cancer that receive trastuzumab treatment. [ABSTRACT FROM AUTHOR]

The aim of the present study was to analyze the mechanism by which nerve growth factor (NGF) promotes callus formation in mice with tibial fracture. NGF transgenic homozygotic mice and NGF wild homozygotic mice were selected to construct non-stabilized fracture model of tibia. The mice were sacrificed on days 7, 14 and 21, respectively, and each group had a sample with 8 mice at each point in time. X-ray radiography and safranin fast green were used to observe fracture healing and in situ hybridization was used to examine the NGF mRNA expression of tibia at each phase of fracture healing. Tartrate-resistant acid phosphatase (TRAP) staining of callus tissue and the expression level of TRAP mRNA were combined to observe osteoclast formation. COL2A1, a chondrocyte differentiation-related gene in callus, and the mRNA level of SOX9 were combined to observe chondrocyte differentiation. It was found that under X-ray radiography, the fracture of NGF transgenic homozygotic mice healed in advance (P<0.05). Cartilage and bone tissue were identified by safranin and fast green staining. The residual cartilage on the callus tissue of NGF transgenic homozygotic mice had decreased significantly (P<0.05). The NGF mRNA expression level in each phase of callus formation of NGF transgenic homozygotic mice was significantly higher than that of the wild group (P<0.05). The number of positive cells in NGF-TRAP staining at each time point after fracture and the NGF mRNA expression level was markedly higher than that of the wild group, and the expression levels of COL2A1 and SOX9 mRNA were distinctively higher than that of the wild group. In conclusion, NGF potentially improves the healing of tibial fracture by osteoclast formation. Additionally, an increase in the number of osteoblasts in the NGF transgenic homozygotic mice compared with the wild-type mice may be achieved by cartilage differentiation due to NGF increasing the COL2A1 and SOX9 mRNA expression levels. [ABSTRACT FROM AUTHOR]

The goal of the present study was to examine the characteristics of carbapenem-resistant Klebsiella pneumoniae as a cause of neonatal infection. A total of 37 carbapenem-resistant Klebsiella pneumoniae-positive newborns hospitalized in Shandong Provincial Hospital, China between April 2011 and October 2013 were examined. Antibiotic susceptibility testing was performed using the agar dilution method and the Etest. Resistance genes were assessed by polymerase chain reaction (PCR) and sequencing. Pulsed-field gel electrophoresis (PFGE) and multi-locus sequence typing (MLST) were used to determine the genotypes and homology of these isolates. Plasmids were analyzed by PFGE and conjugation experiments. The outer membrane proteins were examined by PCR and SDS-PAGE. All of the isolates were revealed to be resistant to the third and fourth generation cephalosporins and piperacillin-tazobactam. Tigecycline, colistin, levofloxacin and amikacin were successful against all of the isolates. The antibiotic resistance rates of aztreonam, gentamicin, trimethoprim-sulfamethoxazole and fosfomycin were 13.51, 48.64, 78.38 and 86.49%, respectively. Of the 37 cases, 25 isolates (67.57%) were blaNDM-1 positive, 13 isolates (35.14%) were blaIMP-4 positive and 1 isolate (2.70%) was blaIMP-8 positive. Two isolates carried both blaNDM-1 and blaIMP-4. The isolate carrying 2-4 plasmids and blaNDM-1 and blaIMP-4 was transferable between strains. SDS-PAGE data indicated that outer membrane proteins remained present. PFGE revealed 7 distinct clusters, and MLST reported the presence of ST20, ST17, ST54, ST705 and ST290 sequences, which indicated that there was clone and plasmid spread between newborns. The main resistance mechanism of carbapenem-resistant Klebsiella pneumoniae was that the isolates expressed the carbapenemase resistance of blaNDM-1 and blaIMP-4 genes. The current study indicates that early detection of these genes may be helpful in infection prevention and control. [ABSTRACT FROM AUTHOR]

Intestinal pseudo-obstruction (IpsO) and acute lupus pneumonitis (ALP) are uncommon severe complications of systemic lupus erythematosus (SLE). The present study reports the case of a 26-year-old female who presented with abdominal pain, nausea and vomiting as initial symptoms. Computed tomography (CT) scanning revealed the jejunal wall was thickened and streaky, mimicking the presentation of intestinal obstruction. Following emergency surgery, the patient's general condition was aggravated, with evident limb erythematous rashes. A series of laboratory examinations revealed SLE, and combined with patient's medical history IpsO was diagnosed, with a disease Activity Index score of 10. During the therapeutic period, high fever, dyspnea and oxygen saturation (SaO2) reductions were detected, and CT scans indicated lung infiltration, excluding other causes through a comprehensive infectious work-up and a bronchoalveolar lavage examination. ALP was confirmed and treated with high-dose methylprednisolone and gamma globulin supplement. The patient responded well and was discharged in 2 weeks. In the one-year tapering period and after stopping corticosteroids, the patient recovered well with no relapse detected. In conclusion, the manifestation of IpsO in SLE is rare and represents a challenge for the surgeon to establish the correct diagnosis and avoid inappropriate surgical intervention. ALP may be the consequence of emergency surgery, and immediate high-dose glucocorticoid therapy is recommended. [ABSTRACT FROM AUTHOR]

Insulin is used in the treatment of type 2 diabetes, with its usage reaching 30-50% in Western countries. The aim of the present study was to determine the association between insulin dosage (ID)/insulin usage time (IT) and coronary artery lesions in patients of type 2 diabetes with coronary heart disease. Based on the insulin using dosage, 353 type 2 diabetes patients were divided into the high-dose (≥0.5 IU/kg) and low-dose (<0.5 IU/kg) group. Selected coronary angiography was performed and the Gensini score was used to determine the degree of the coronary artery lesions. The homeostasis model assessment-insulin sensitivity (HOMA-IS) index was assessed by HOMA2. Data including age, gender, smoking, body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC), triglyceride (TG), glucose (Glu), hemoglobin A1c (HbA1c), C-peptide, ID, IT, diabetes duration time (DT), and IT/DT were collected. The association between insulin usage (both dose and time) and the coronary artery lesions in these patients was then determined. Statistical differences for the two groups for factors including C-peptide, HbA1c, ID, IT, DT, IT/DT and the Gensini score values (P<0.05) were identified. By contrast, no significant differences for factors such as gender, smoking history, age, BMI, TC, TG, LDL, HDL, fasting insulin, Glu, SBP and DBP were observed. The coronary artery damage Gensini score in insulin-insensitive individuals was significantly greater than that in the insulin-sensitive individuals. The Spearman analysis revealed that ID and IT, DT and IT/DT were positively correlated with the coronary artery damage Gensini score. The multivariate regression, the interquartile range method and receiver operating characteristic analyses showed that ID, ID/DT, IT had a greater effect on coronary vascular damage compared with DT. In conclusion, the degree of coronary artery lesions were correlated with ID, IT, DT, IT/DT. High doses of insulin or a high IT/DT ratio may aggravate coronary artery damage. [ABSTRACT FROM AUTHOR]

Off-pump coronary artery bypass (OPCAB) surgery is the most effective treatment for coronary heart disease. The aim of this study was to explore the effects of OPCAB on the basis of the associated molecular mechanisms. GSE12486 expression profiles downloaded from the Gene Expression Omnibus database (GEO) were analyzed to identify the differentially expressed genes (DEGs). Principal component analysis (PCA) was conducted based on the expression profiles of DEGs. Function and pathway enrichment of upregulated DEGs was performed, followed by protein-protein interaction (PPI) network construction. Gene Set Enrichment Analysis (GSEA) was used for miRNA enrichment analysis based on expression profiles and prediction of their association with the disease. Cytoscape was applied to construct miRNA regulatory networks of DEGs. In total 64 DEGs were identified, including 63 upregulated and 1 downregulated gene. The first principal component in the PCA analysis was able to distinguish between pre- and post-OPCAB samples. Upregulated DEGs mainly enriched 20 Gene Ontology terms, such as chemokine activity, and 5 pathways including the chemokine signaling pathway. The constructed PPI network contained 234 edges and 55 nodes, and 10 upregulated hub nodes, including FBJ murine osteosarcoma viral oncogene homolog (FOS), were screened. A total of 36 miRNAs, including MIR-224 and MIR-7, were screened by GSEA enrichment analysis. A miRNA regulatory network including 176 edges and 97 nodes was constructed, showing the regulatory relationships between miRNAs and DEGs. For example, early growth response 2 (EGR2) was regulated by 8 miRNAs including MIR-150, MIR-142-3P, MIR-367 and MIR-224. The identified DEGs might play important roles in patients pre- and post-OPCAB surgery via the regulation of associated genes. [ABSTRACT FROM AUTHOR]

The aim of the present study was to detect the expression of resistin in rats with acute pancreatitis (AP) and investigate its significance in the pathogenesis of AP. In total, 40 Sprague-Dawley rats were randomly divided into four groups (n=10), including the normal control, sham-operated, acute edematous pancreatitis (AEP) and acute necrotizing pancreatitis (ANP) groups. Following the establishment of animal models, the levels of serum resistin, C-reactive protein (CRP), tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β were measured using ELISA. Resistin expression in the pancreatic tissues was detected using an immunohistochemical method. In addition, the mRNA expression of resistin in the pancreatic tissues was analyzed with quantitative polymerase chain reaction. The levels of serum amylase, serum resistin, TNF-α, IL-1β and CRP were all significantly higher in the AEP and ANP groups when compared with the control and sham-operated groups (P<0.01), as were the pancreas/body weight ratios and pathological scores of the pancreas. These increases were more significant in the ANP group than in the AEP group (P<0.05). The mRNA expression levels of resistin in the pancreatic tissues were markedly higher in the AEP and ANP groups when compared with the control and sham-operated groups (P<0.01), particularly in the pancreatic tissues of the ANP group, which exhibited notably higher levels compared with the AEP group. The serum resistin level was found to positively correlate with the serum levels of CRP, TNF-α and IL-1β, and the pathological scores of the pancreatic tissues. In conclusion, the results indicated that resistin may be associated with the occurrence and development of AP; thus, the protein may be a valuable indicator for assessing the severity of AP. [ABSTRACT FROM AUTHOR]

The objective of the present study was to comparatively investigate the feasibility and safety of etomidate and propofol use following sevoflurane inhalation in autistic children during the intrathecal transplantation of stem cells. The patients selected were 60 autistic children with American Society of Anesthesiologists physical status I, who were aged between two and 12 years and scheduled for stem cell transplantation. The children received an inhalation induction of 8% sevoflurane, followed by intravenous injection of etomidate (0.2 mg/kg) in group E and propofol (2 mg/kg) in group P (n=30/group). Supplemental doses of 0.1 mg/kg etomidate or 1 mg/kg propofol were used until a deep sedation was obtained. The heart rate (HR), mean arterial pressure, oxygen saturation, respiratory rate, Ramsay sedation score (RSS) and recovery time were monitored continuously. Following anesthesia, blood pressure and HR measurements were significantly decreased in group P compared with the baseline (P<0.01) and group E values at the same time-points (P<0.05). The occurrence of adverse effects, such as respiratory depression, bradycardia, hypotension and pain on injection, was significantly higher in group P than that in group E, whereas the incidence of myoclonus in group E was significantly higher than that in group P (P<0.01). No significant differences in anesthesia induction, surgery duration, recovery time, RSS and physician satisfaction were observed between the two groups. In conclusion, sevoflurane-etomidate combinations resulted in more stable hemodynamic responses and relatively fewer adverse effects compared with propofol injection following sevoflurane inhalation and may therefore be more suitable for the induction of short-term anesthesia in autistic children during stem cell transplantation. [ABSTRACT FROM AUTHOR]

Although classified as benign, giant cell tumors of the bone (GCTB) may be aggressive, recur and even metastasize to the lungs. In addition, the pathogenesis and histogenesis remain unclear; thus, the driving factors behind the strong tumor growth capacity of GCTB require investigation. In the present study, the expression levels of hypoxia-inducible factor (HIF)-1α and vascular endothelial growth factor (VEGF), which are promoted by hypoxic conditions, were determined in 22 sacral GCTB samples using immunohistochemistry and western blot analysis. Furthermore, CD34 expression was analyzed using these methods. The correlation between HIF-1α or VEGF expression and the tumor microvessel density (MVD) was then determined. The results demonstrated that HIF-1α, VEGF and CD34 were overexpressed in the 22 sacral GCTB specimens, and overexpression of HIF-1α and VEGF correlated with the tumor MVD. Thus, the present study has provided novel indicators for the tumor growth capacity of GCTBs. [ABSTRACT FROM AUTHOR]

Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) have pivotal functions in extracellular matrix turnover and are involved in chronic kidney diseases. However, the exact functions of MMPs in chronic renal failure (CRF) have yet to be demon-strated. The aim of the present study was to examine the effects of MMP-9 on CRF. An adenine-induced model of CRF was generated in rabbits. Following the injection of MMP 9 into the renal arteries of the rabbits, significant improvements in renal morphology and serum levels of creatinine and urea nitrogen were observed. Furthermore, MMP-9 administration was shown to decrease the serum TIMP-1 concentration and upregulate renal MMP-9 expression. These results demonstrate a directly protective role for MMP-9 in CRF. [ABSTRACT FROM AUTHOR]