Zhang L.,Ordos Central Hospital
International Eye Science | Year: 2016
AIM: To analyze effect of the inside incision positions of clear corneal incisions of cataract on astigmatism after surgery was analysis using anterior segment optical coherence tomography. METHODS: A total of 40 patients of 43 eyes of age-related cataract were chosen. All of them were done 2.8 mm clear corneal incision and phacoemulsification with foldable intraocular lens implantation. Preoperative and postoperative 1 wk, 1 and 3 mo, the corrected visual acuity were examined. Postoperative 1 wk, 1 and 3 mo, the positions and lengths of the incisions were measured. Depending on the location of the incisions, the patients were divided into two groups. Group 1: the inside mouth of the incisions (22 patients of 23 eyes) were far from the corneal vertex central line >3 mm. Group 2: the inside mouth of the incisions (20 patients of 20 eyes) were far from the corneal vertex central line ≤3 mm. RESULTS: One day before the surgery between Group 1 and Group 2 patients, there were no statistically significant difference (PP>0.05) in corrected visual acuity and corneal astigmatism. After the surgery, corrected visual acuity gradually increased, astigmatism and cut lengths gradually decreased. But, there were no statistically significant difference at 1 wk, 1 and 3 mo (P<0.05). CONCLUSION: The length of the inside mouth located within radius of the central cornea 3 mm was rather longer than the length of the inside mouth located without radius of the central cornea 3 mm.The SIA after surgery is greater, and postoperative visual acuity gained maybe less than the latter. Copyright 2016 by the IJO Press.
Liu Y.,Peking University |
Liu Y.,CAS National Center for Nanoscience and Technology |
Feng J.,CAS National Center for Nanoscience and Technology |
Shi L.,306 Hospital |
And 7 more authors.
Nanoscale | Year: 2012
Nanomechanical behaviors of single living cardiomyocytes are quantitatively observed using calculated torsions and deflections of an AFM cantilever. The lateral contractions are related to the calcium intensity within rather than the vertical beating power of the cardiomyocytes. Drug-induced nanomechanical changes of cardiomyocytes were further investigated by measuring lateral contractions in real time.
Wang Y.,Liaoning Medical University |
Liu N.,Ordos Central Hospital |
Su X.,Liaoning Medical University |
Zhou G.,Liaoning Medical University |
And 4 more authors.
Biomedicine and Pharmacotherapy | Year: 2015
Transforming growth factor-β1 (TGF-β1) induced epithelial-mesenchymal transition (EMT) plays an important role in renal fibrotic process regulation. Epigallocatechin-3-gallate (EGCG) exerts a protective effect against acute renal damage through its anti-oxidative effect by activating the Nrf2 signaling pathway. This study aims to investigate whether EGCG prevents TGF-β1 induced EMT and whether this effect acts via the Nrf2-mediated suppression of TGF-β1 signaling. MTT was used for cytotoxicity of EGCG examination and Western blotting and immunofluorescence were used for protein expression analysis. Results showed that EGCG prevented TGF-β1 mediated EMT and Smad 2 and Smad 3 phosphorylation in a dose dependent manner in NRK-52E cells. In addition, EGCG increased Nrf2 nuclear accumulation. Overexpression of Nrf2 blocked the phosphorylation of Smad 2 and Smad 3 mediated by TGF-β1 and decreased protein expression of plasminogen activator inhibitor 1 (PAI-1) and α-smooth muscle actin (α-SMA). Furthermore, siRNA-mediated knockdown of Nrf2 gene completely blocked the effects of EGCG, indicated by the reduced expressions of type I collagen (Col-I) and α-SMA were restored. In summary, EGCG inhibits TGF-β1 induced EMT and fibrotic proteins expression by Nrf2 activation. This study reveals a possible underlying mechanism of the renal protective effects of EGCG, and may provide a potential candidate to renal fibrosis therapy. © 2015 Elsevier Masson SAS.
Wang Y.,Shenyang University |
Wang B.,Shenyang University |
Du F.,Shenyang University |
Su X.,Shenyang University |
And 4 more authors.
Basic and Clinical Pharmacology and Toxicology | Year: 2015
Oxidative stress and inflammation contribute importantly to the pathogenesis of chronic kidney disease (CKD). Epigallocatechin-3-gallate (EGCG), which is the most abundant and most active catechin polyphenol extracted from green tea, has been proved to have many bioactivities. In this study, the renoprotective effect of EGCG was evaluated in a widely used kidney disease model, the unilateral ureteral obstruction (UUO) mice model. After 14 days of EGCG administration, mean arterial blood pressure, body-weight and obstructed kidney weight were measured. Levels of blood urea nitrogen (BUN) and creatinine (CR) and activities of glutamic-pyruvic transaminase (GPT) and lactate dehydrogenase (LDH) in serum were estimated as indicators of renal function. Periodic acid-Schiff (PAS) staining was performed to observe the pathological changes of the obstructed kidney. Antioxidant enzymes and pro-inflammatory cytokine production were estimated to reflect the oxidative stress and inflammatory state in the obstructed kidney. Finally, the main proteins in the NF-κB and Nrf2 signalling pathway and DNA binding activity of NF-κB and Nrf2 were measured to investigate the effect of EGCG on these two pathways. The results demonstrated that EGCG could restore UUO-induced kidney weight loss and renal dysfunction. In addition, UUO-induced oxidative stress and inflammatory responses in the obstructed kidney were also prevented by EGCG. Furthermore, EGCG could induce both NF-κB and Nrf2 nuclear translocation in the UUO kidney and promote heme oxygenase-1 (HO-1) production. These results indicated that the renoprotective effect of EGCG might be through its NF-κB and Nrf2 signalling pathway regulations. © 2015 Nordic Association for the Publication of BCPT (former Nordic Pharmacological Society).
Wang Y.,Shengjing Hospital of China Medical University |
Wang B.,Shengjing Hospital of China Medical University |
Du F.,Shengjing Hospital of China Medical University |
Su X.,Shengjing Hospital of China Medical University |
And 4 more authors.
Journal of Histochemistry and Cytochemistry | Year: 2015
The severity of tubulointerstitial fibrosis is regarded as an important determinant of renal prognosis. Therapeutic strategies targeting tubulointerstitial fibrosis have been considered to have potential in the treatment of chronic kidney disease. This study aims to evaluate the protective effects of (-)-epigallocatechin-3-gallate (EGCG), a green tea polyphenol, against renal interstitial fibrosis in mice. EGCG was administrated intraperitoneally for 14 days in a mouse model of unilateral ureteral obstruction (UUO). The results of our histological examination showed that EGCG alleviated glomerular and tubular injury and attenuated renal interstitial fibrosis in UUO mice. Furthermore, the inflammatory responses induced by UUO were inhibited, as represented by decreased macrophage infiltration and inflammatory cytokine production. Additionally, the expression of type I and III collagen in the kidney were reduced by EGCG, which indicated an inhibition of extracellular matrix accumulation. EGCG also caused an up-regulation in α-smooth muscle actin expression and a down-regulation in E-cadherin expression, indicating the inhibition of epithelial-to-mesenchymal transition. These changes were found to be in parallel with the decreased level of TGF-β1 and phosphorylated Smad. In conclusion, the present study demonstrates that EGCG could attenuate renal interstitial fibrosis in UUO mice, and this renoprotective effect might be associated with its effects of inflammatory responses alleviation and TGF-β/Smad signaling pathway inhibition. © The Author(s) 2015
PubMed | Ordos Central Hospital and Capital Medical University
Type: Journal Article | Journal: The journal of obstetrics and gynaecology research | Year: 2016
Post-partum hemorrhage (PPH) is a common complication of cesarean sections (CS) and affects maternal and newborn health. We used a new method to control bleeding and compared its efficacy with conventional methods.Eighty-six women who experienced PPH with volume of bleeding over 1000 mL in CS between January 2008 and January 2012 were chosen as samples. Thirty-three underwent the new method in which normal saline ice blocks are placed in the uterus, and 53 underwent the conventional method. We evaluated blood loss, volume of transfusion and complications.Patients who were treated with ice blocks had better hemostatic efficacy than those who underwent the conventional method (1450 251.9mL vs 1800 278.9 mL; P < 0.001); they also had less blood transfusion (806.1 242.3mL vs 1222.6 308.0 mL; P < 0.001), lower rate of hysterectomy and infection (3.03% vs 5.66%; P = 0.971; 0% vs 7.55%; P = 0.276), and shorter duration of hospital stay (5.3 0.5days vs 7.6 3.0 days; P < 0.001).PPH in CS can be treated with peeled sterile normal saline ice blocks, a simple and reliable method for stopping bleeding. Nonetheless, there needs to be a large randomized control trial for confirmation.
PubMed | Ordos Central Hospital and Liaoning Medical University
Type: | Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie | Year: 2015
Transforming growth factor-1 (TGF-1) induced epithelial-mesenchymal transition (EMT) plays an important role in renal fibrotic process regulation. Epigallocatechin-3-gallate (EGCG) exerts a protective effect against acute renal damage through its anti-oxidative effect by activating the Nrf2 signaling pathway. This study aims to investigate whether EGCG prevents TGF-1 induced EMT and whether this effect acts via the Nrf2-mediated suppression of TGF-1 signaling. MTT was used for cytotoxicity of EGCG examination and Western blotting and immunofluorescence were used for protein expression analysis. Results showed that EGCG prevented TGF-1 mediated EMT and Smad 2 and Smad 3 phosphorylation in a dose dependent manner in NRK-52E cells. In addition, EGCG increased Nrf2 nuclear accumulation. Overexpression of Nrf2 blocked the phosphorylation of Smad 2 and Smad 3 mediated by TGF-1 and decreased protein expression of plasminogen activator inhibitor 1 (PAI-1) and -smooth muscle actin (-SMA). Furthermore, siRNA-mediated knockdown of Nrf2 gene completely blocked the effects of EGCG, indicated by the reduced expressions of type I collagen (Col-I) and -SMA were restored. In summary, EGCG inhibits TGF-1 induced EMT and fibrotic proteins expression by Nrf2 activation. This study reveals a possible underlying mechanism of the renal protective effects of EGCG, and may provide a potential candidate to renal fibrosis therapy.
PubMed | Ordos Central Hospital and Inner Mongolia University
Type: Journal Article | Journal: Experimental and therapeutic medicine | Year: 2016
The present study aimed to investigate whether genetic polymorphisms in the Toll-like receptor (TLR)-4 and Toll/interleukin-1 receptor (TIR)-associated protein (TIRAP) genes, and/or their expression levels, influence the susceptibility of a patient to sepsis. A total of 106 patients with sepsis were divided into two groups on the basis of their acute physiology and chronic health evaluation (APACHE) II scores: i) Sepsis group A (APACHE II <20) and ii) Sepsis group B (APACHE II >20). In addition, 100 healthy volunteers were enrolled into the control group. Polymerase chain reaction-restriction fragment length polymorphism assay was used to detect the following genetic polymorphisms: The Ser180Leu allele of the TIRAP gene and the Asp299Gly and Thr399I1e alleles of the TLR4 gene. Furthermore, the protein expression levels of TLR4 and TIRAP were analyzed using an enzyme-linked immunosorbent assay. Genetic polymorphisms were not detected for the TLR4 and TIRAP genes; however, the protein expression levels of TLR4 and TIRAP differed significantly between the control, sepsis A and sepsis B groups (P<0.01). An APACHE II score of 20 was used as a baseline in order to differentiate sepsis severity. Pearson analysis demonstrated that TLR4 and TIRAP protein expression levels were positively correlated with sepsis severity (
PubMed | Renshou County Peoples Hospital, Hebei Medical University, Nanjing Southeast University, Hangzhou Hospital of Traditional Chinese Medicine and 38 more.
Type: Journal Article | Journal: Lancet (London, England) | Year: 2015
Acute kidney injury (AKI) has become a worldwide public health problem, but little information is available about the disease burden in China. We aimed to evaluate the burden of AKI and assess the availability of diagnosis and treatment in China.We launched a nationwide, cross-sectional survey of adult patients who were admitted to hospital in 2013 in academic or local hospitals from 22 provinces in mainland China. Patients with suspected AKI were screened out on the basis of changes in serum creatinine by the Laboratory Information System, and we reviewed medical records for 2 months (January and July) to confirm diagnoses. We assessed rates of AKI according to two identification criteria: the 2012 Kidney Disease: Improving Global Outcomes (KDIGO) AKI definition and an increase or decrease in serum creatinine by 50% during hospital stay (expanded criteria). We estimated national rates with data from the 2013 report by the Chinese National Health and Family Planning Commission and National Bureau of Statistics.Of 2,223,230 patients admitted to the 44 hospitals screened in 2013, 154,950 (70%) were suspected of having AKI by electronic screening, of whom 26,086 patients (from 374,286 total admissions) were reviewed with medical records to confirm the diagnosis of AKI. The detection rate of AKI was 099% (3687 of 374,286) by KDIGO criteria and 203% (7604 of 374,286) by expanded criteria, from which we estimate that 14-29 million people with AKI were admitted to hospital in China in 2013. The non-recognition rate of AKI was 742% (5608 of 7555 with available data). Renal referral was done in 214% (1625 of 7604) of the AKI cases, and renal replacement therapy was done in 593% (531 of 896) of those who had the indications. Delayed AKI recognition was an independent risk factor for in-hospital mortality, and renal referral was an independent protective factor for AKI under-recognition and mortalityAKI has become a huge medical burden in China, with substantial underdiagnosis and undertreatment. Nephrologists should take the responsibility for leading the battle against AKI.National 985 Project of China, National Natural Science Foundation of China, Beijing Training Program for Talents, International Society of Nephrology Research Committee, and Bethune Fund Management Committee.
PubMed | Ordos Central Hospital and Liaoning Medical University
Type: Evaluation Studies | Journal: The Journal of surgical research | Year: 2015
Tubular cell apoptosis plays a crucial role in different kinds of renal diseases. Epigallocatechin-3-gallate (EGCG), a polyphenol extracted from green tea, has been shown to inhibit renal fibrosis in unilateral ureteral obstruction (UUO) mice, but its role in preventing tubular cell apoptosis and the underlying signaling mechanisms still remains unclear.Mice subjected to UUO were intraperitoneally administered EGCG (5 mg/kg) for 14 d. Normal rat kidney proximal tubular epithelial cell line NRK-52E was induced by transforming growth factor 1 (TGF-1). Periodic acid-schiff and Massons trichrome staining was used for histologic study. TUNEL, Hoechst staining, and flow cytometry analysis were used to measure the apoptotic status of tubular cells. Western blotting was used to determine the expression of apoptotic-associated proteins and mitogen-activated protein kinase pathway proteins.EGCG significantly attenuated tubular injury and renal tubulointerstitial fibrosis in the obstructed kidneys of UUO mice. In addition, EGCG prevented UUO and TGF-1-induced tubular apoptosis in a dose-dependent manner. In parallel, protein expression of B-clell lymphoma-2 (Bcl-2) was upregulated and protein expressions of Bcl-2 accosiated X protein (Bax), cleaved caspase 3, and cleaved poly ADP-ribose polymerase (PARP) were downregulated by EGCG. Furthermore, UUO and TGF-1-stimulated phosphorylation of mitogen-activated protein kinase was inhibited by EGCG.EGCG effectively reduces tubular cell apoptosis induced by UUO and may have potential as a clinical treatment in patients with chronic kidney disease.