Zhi Zheng

Hangzhou First People's Hospital, Hang-hsien, Zhejiang Sheng, China

Are you Zhi Zheng?

Claim your profile

Publications (36)73.56 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Diabetic retinopathy (DR) is a major cause of blindness in the working-age populations of developed countries, and effective treatments and prevention measures have long been the foci of study. Patients with DR invariably demonstrate impairments of the retinal microvascular endothelium. Many observational and preclinical studies have shown that angiogenesis and apoptosis play crucial roles in the pathogenesis of DR. Increasing evidence suggests that in DR, the small guanosine-5'-triphosphate-binding protein RhoA activates its downstream targets mammalian Diaphanous homolog 1 (mDia-1) and profilin-1, thus affecting important cellular functions, including cell morphology, motility, secretion, proliferation, and gene expression. However, the specific underlying mechanism of disease remains unclear. This review focuses on the RhoA/mDia-1/profilin-1 signaling pathway that specifically triggers endothelial dysfunction in diabetic patients. Recently, RhoA and profilin-1 signaling has attracted a great deal of attention in the context of diabetes-related research. However, the precise molecular mechanism by which the RhoA/mDia-1/profilin-1 pathway is involved in progression of microvascular endothelial dysfunction (MVED) during DR has not been determined. This review briefly describes each feature of the cascade before exploring the most recent findings on how the pathway may trigger endothelial dysfunction in DR. When the underlying mechanisms are understood, novel therapies seeking to restore the endothelial homeostasis comprised in DR will become possible.
    Albrecht von Graæes Archiv für Ophthalmologie 03/2015; 253(5). DOI:10.1007/s00417-015-2985-3 · 2.33 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: A thin and flexible paper-based skin patch was developed for the diagnostic screening of Cystic Fibrosis. It utilized a unique combination of anion exchange and pH testing papers to enable a quantitative, colorimetric and on-skin detection for sweat anions.
    Chemical Communications 03/2015; DOI:10.1039/C5CC00717H · 6.72 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The aim of this study was to evaluate the embolic sequelae of left atrial myxomas and their influence on diagnosis, treatment, and prognosis. Seventy-eight patients were retrospectively investigated. According to their symptoms and neurologic-imaging findings, these patients were classified into 2 groups: embolism (15 patients, 19%) and nonembolism (63 patients, 81%). The time from the first onset of symptoms to diagnosis (that is, the duration of symptoms) was significantly longer in the embolism group than in the nonembolism group (105 ± 190 vs 23 ± 18 d; P <0.01). The myxomas were divided into 2 types on the basis of clinicopathologic findings: type 1, with an irregular or villous surface and a soft consistency, and type 2, with a smooth surface and a compact consistency. There were 42 patients with type 1 myxoma and 36 with type 2. Type 1 myxoma was more frequently found in the embolism group (12 patients, 29%) than was type 2 myxoma (3 patients, 8%). The difference was significant (P=0.04). There were 2 perioperative deaths in the nonembolism group. No recurrence of cardiac myxoma or death was recorded in either group during follow-up. In the embolism group, neurologic symptoms were relieved by surgery, and no subsequent neurologic event was reported. Because surgical resection is highly effective in left atrial myxoma, we should strive for early diagnosis in order to shorten the duration of symptoms and to avoid worse neurologic damage in patients in whom an embolic event is the initial manifestation.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective: Purpose of this study was to validate that Subtenon (SB) Triamcinolone (TA) injection is an alternative to Intravitreal (IV) Triamcinolone (TA) injection for the treatment of diabetic macular edema (DME). Methods: Forty eyes were selected having DME due to type 1 or type 2 diabetes. All the patients were treated with photocoagulation. IVTA was administered in one eye and SBTA in following eye of same patient. Improvement in visual acuity, macular edema and intraocular pressure was assessed before treatment and on 2nd, 4th, 8th and 12th week after treatment. Results: After administration of IVTA, MVA was reduced from baseline value (0.805 ± 0.069Log/MAR) to (0.577 ± 0.091 Log/MAR, p<.001) at the end of treatment. Similar results were observed after SBTA administration. MVA was reduced from (0.814 ± 0.082Log/MAR) to (0.49 ± 0.080 Log/MAR, p<.001) at 12th week. After IVTA injection Central macular thickness was significantly reduced to (246.8 ± 25 µm, p<0.001) from (390.5 ± 17 µm). There were no significant (p=0.51) difference in both eyes receiving different routes of same treatment. After SBTA injection CMT was significantly reduced to lower values (241.5 ± 27 µm, p<0.001) from (394.4 ± 21 µm). Intraocular pressure after IVTA administration was high (2.32 ± 0.72 mm/Hg, p=0.04) as compared to baseline (1.82 ± 0.94 mm/Hg). Similar pattern was also seen after SBTA administration but to significant extent. Elevation of IoP was observed in both eyes. Conclusion: Subtenon Triamcinolone injection is an alternative to Intravitreal Triamcinolone Injection for Diabetic Macular Edema.
    Pakistan Journal of Medical Sciences Online 07/2014; 30(4):749-54. DOI:10.12669/pjms.304.4810 · 0.10 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Hepatitis C virus (HCV) infection is a serious and rising global healthcare problem. One critical challenge to tackle this disease is the lack of adequate diagnosis. Here, we develop a multiplex microfluidic paper-based immunoassay, as a novel diagnostic approach, to detect human IgG antibody against HCV (anti-HCV). The paper substrate, highly flammable Nitrocellulose (NC), is patterned under ambient temperature by Craft Punch Patterning (CPP) to generate multiple test zones. On the basis of superior merits of patterned paper, this new diagnostic approach demonstrates the key novelty to unprecedentedly combine segmented diagnostic assays into a single multiplex test. The generated diagnostic results are not only informative, but can be rapidly and cost-effectively delivered. It would significantly transform clinical pathway for unwitting individuals with HCV infection. This work highlights the promising role of microfluidic paper-based immunoassay in tackling the diagnostic challenge for HCV pandemic as well as the innovation of diagnostics in other diseases.
    Analytical Chemistry 05/2014; 86(11). DOI:10.1021/ac500247f · 5.83 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: To develop a reliable, reproducible rat model of retinal vein occlusion (RVO) with a novel photosensitizer (erythrosin B) and study the cellular responses in the retina. Central and branch RVOs were created in adult male rats via photochemically-induced ischemia. Retinal changes were monitored via color fundus photography and fluorescein angiography at 1 and 3h, and 1, 4, 7, 14, and 21d after irradiation. Tissue slices were evaluated histopathologically. Retinal ganglion cell survival at different times after RVO induction was quantified by nuclear density count. Retinal thickness was also observed. For all rats in both the central and branch RVO groups, blood flow ceased immediately after laser irradiation and retinal edema was evident at one hour. The retinal detachment rate was 100% at 3h and developed into bullous retinal detachment within 24h. Retinal hemorrhages were not observed until 24h. Clearance of the occluded veins at 7d was observed by fluorescein angiography. Disease manifestation in the central RVO eyes was more severe than in the branch RVO group. A remarkable reduction in the ganglion cell count and retinal thickness was observed in the central RVO group by 21d, whereas moderate changes occurred in the branch RVO group. Rat RVO created by photochemically-induced ischemia using erythrosin B is a reproducible and reliable animal model for mimicking the key features of human RVO. However, considering the 100% rate of retinal detachment, this animal model is more suitable for studying RVO with chronic retinal detachment.
    International Journal of Ophthalmology 04/2014; 7(2):232-238. DOI:10.3980/j.issn.2222-3959.2014.02.08 · 0.50 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Studies have shown that an overproduction of mitochondrial reactive oxygen species (ROS) is an initiating cause in the pathogenesis of diabetic complications. However, uncoupling protein 2 (UCP2) can protect retinal vascular endothelial cells from damage by inhibiting the overproduction of mitochondrial ROS, although the protective mechanism involved is not completely clear. This study aimed to assess the effect and mechanism of UCP2 on the apoptosis of human umbilical vein endothelial cells (HUVECs). HUVECs were cultured in normal glucose (NG, 5.5 mmol/l) or high glucose (HG, 30 mmol/l) medium in the presence or absence of UCP2+/+ lentiviral transfection. Lentivirus-mediated UCP2 overexpression inhibited the apoptosis of HUVECs induced by HG. Treatment with HG resulted in the upregulation of caspase-3 and cytochrome c and the downregulation of Bcl-2 in vitro. Furthermore, compared with the NG group, the rate of apoptosis was significantly increased in the HG group. On day two post-infection, NG cells showed significantly greater HUVEC cell proliferation than HG cells. Notably, UCP2 overexpression inhibited these processes. Taken together, these results suggest that UCP2 promotes cell proliferation and inhibits HG-induced apoptosis in HUVECs via the Bcl-2 up‑ and downregulation of caspase-3 and cytochrome c in vitro. This may provide experimental evidence for the application of UCP2 as a new protective factor for diabetic complications, such as diabetic retinopathy.
    International Journal of Molecular Medicine 02/2014; 33(5). DOI:10.3892/ijmm.2014.1676 · 1.88 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Diabetic retinopathy (DR) is a well-known serious complication of diabetes mellitus (DM), and can eventually advance to end-stage blindness. In the early stage of DR, endothelial cell barrier disorganized primarily and tight junction (TJ) protein composition transformed subsequently. The small GTPase RhoA and its downstream effector Rho-associated coiled-coil containing protein kinase 1 (ROCK1) regulate a mass of cellular processes, including cell adherence, proliferation, permeability and apoptosis. Although RhoA inhibitors have provided substantial clinical benefit as hypertonicity therapeutics, their use is limited by complex microenvironment as DR. While ample evidence indicates that TJ can be influenced by the RhoA/ROCK1 signaling, the underlying mechanisms remain incompletely understood. Here, we have uncovered a significant signaling network involved in diabetic retinal microvascular endothelial dysfunction (RMVED). Our results indicated that the activation of RhoA/ROCK1 pathway due to high glucose played a key role in microvascular endothelial cell dysfunction (MVED) by way of directly inducing TJ proteins over-expression during DR. We demonstrated that inhibition of RhoA/ROCK1 may attenuate the hypertonicity of endothelial cell caused by high glucose microenvironment meanwhile. Besides, chemical and pharmacological inhibitors of RhoA/ROCK1 pathway may partly block inflammation due to DR. Simultaneously, the apoptosis aroused by high glucose was also prevented considerably by fasudil, a kind of pharmacological inhibitor of RhoA/ROCK1 pathway. These findings indicate that RhoA/ROCK1 signaling directly modulates MVED, suggesting a novel therapeutic target for DR.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Fluidic patterning is a convenient and versatile tool for the patterning of materials, cells and microstructures on surface and in microchannels. However, its performance is usually limited by transverse diffusion between fluid streams. It would blur the boundary and deteriorate the precision of patterns. In this paper, we adopted geometric confinement to generate biphasic parallel flow that is constituted of oil and water. Since there is minimum transverse diffusion in biphasic parallel flow, the performance of fluid patterning is expected to be improved. The results show that the metal (Silver and Chromium) patterns have distinct boundary and well-controlled geometry in comparison with that by conventional laminar flow patterning. Furthermore, the high biocompatibility of oil phase (perfluorodecalin, PFD) enables the precise patterning of viable bacteria inside microchannels. Our work demonstrated a new route of using biphasic parallel flow to patterning, which would serve wide applications in prototyping and research settings.
    Biomedical Microdevices 12/2013; DOI:10.1007/s10544-013-9828-y · 2.77 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: A minimally invasive and repeatable approach for real-time epidermal growth factor receptor (EGFR) mutation surveillance would be highly beneficial for individualized therapy of late stage lung cancer patients whose surgical specimens are often not available. We aim to develop a viable method to detect EGFR mutations in single circulating tumor cells (CTCs). Using a model CTC system of spiked tumor cells in whole blood, we evaluated EGFR mutation determination in single tumor cells enriched from blood. We used magnetic beads labeled with antibody against leukocyte surface antigens to deplete leukocytes and enrich native CTCs independent of epithelial marker expression level. We then used laser cell microdissection (LCM) to isolate individual CTCs, followed by whole-genome amplification of the DNA for exon 19 microdeletion, L858R and T790M mutation detection by PCR sequencing. EGFR mutations were successfully measured in individual spiked tumor cells enriched from 7.5 ml whole blood. Whole-genome amplification provided sufficient DNA for mutation determination at multiple sites. Ninety-five percent of the single CTCs microdissected by LCM (19/20) yielded PCR amplicons for at least one of the three mutation sites. The amplification success rates were 55 % (11/20) for exon 19 deletion, 45 % (9/20) for T790M, and 85 % (17/20) for L858R. Sequencing of the amplicons showed allele dropout in the amplification reactions, but mutations were correctly identified in 80 % of the amplicons. EGFR mutation determination from single captured tumor cells from blood is feasible with the approach described here. However, to overcome allele dropout and to obtain reliable information about the tumor's EGFR status, multiple individual tumor cells should be assayed.
    Analytical and Bioanalytical Chemistry 07/2013; DOI:10.1007/s00216-013-7156-y · 3.58 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: Although malaria remains as one of the leading infectious diseases in the world, the decline in malaria transmission in some area makes it possible to consider elimination of the disease. As countries approach elimination, malaria diagnosis needs to change from diagnosing ill patients to actively detecting infections in all carriers including asymptomatic and low-parasite load patients. However, few of the current diagnostic methods have both the throughput and the sensitivity required.Methods: We adopted a sandwich RNA hybridization assay to detect genus Plasmodium 18S rRNA directly from the whole blood of Plasmodium falciparum and Plasmodium vivax patients without RNA isolation. We tested the assay with 202 febrile patients from malaria endemic areas, using 20μl of each blood sample in 96-well plate format with a two-day ELISA-like workflow. Results were compared with diagnosis using microscopy, rapid diagnostic test (RDT) and genus specific real time PCR.Results: Our assay identified all 66 positive samples diagnosed by microscopy, including 49 poorly stored samples that underwent multiple freeze-thaw due to resource limitation. The assay uncovered three false-negative samples by microscopy and four false-negative samples by RDT, and agreed completely with real time PCR diagnosis. There was no negative sample by our assay that would show positive when tested with other methods. The detection limit of our assay for P. falciparum was 0.04 parasite/μl.Conclusions: The assay's simple workflow, high throughput and sensitivity make it suitable of active malaria screening.
    Journal of clinical microbiology 01/2013; 51(1):125-130. DOI:10.1128/JCM.02010-12 · 4.23 Impact Factor
  • The American Journal of the Medical Sciences 12/2012; DOI:10.1097/MAJ.0b013e31827487ab · 1.52 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Hyperglycemia-induced vascular cell apoptosis is a seminal early event in diabetic retinopathy. Prolonged hyperglycemia is known to increase intracellular cytosolic free calcium ([Ca(2+)]i) in retinal vascular endothelial cells (RECs), suggesting that [Ca(2+)]i is a critical trigger for microvascular degeneration. This study aims to elucidate Ca(2+)-dependent signaling mechanisms that mediate hyperglycemia-induced apoptosis in RECs. A cultured macaque choroid-retinal endothelial cell line (RF/6A) was incubated in normal glucose (NG), NG plus the Ca(2+) entry blocker 2-aminoethoxydiphenyl borate (2-APB), high glucose (HG), or HG plus either 2-APB, the c-jun N-terminal kinase (JNK) inhibitor SP600125, or the calcium/calmodulin-dependent protein kinase II (CaMKII) inhibitor KN93. Changes in [Ca(2+)]i evoked by adenosine 5'-triphosphate (ATP) were measured in fluo-3/AM-loaded RF/6A cells by confocal microscopy. The mitochondrial membrane potential (ΔΨm) and apoptosis were assessed by flow cytometry. Expression levels of CaMKII, phosphorylated CaMKII (p-CaMKII), c-Jun N-terminal kinase (JNK), phosphorylated JNK (p-JNK), the death receptor (Fas), and cytochrome c were detected by western blotting analysis. Prolonged exposure to HG (96 h) potentiated ATP-evoked Ca(2+) entry as well as CaMKII phosphorylation and RF/6A cell apoptosis. Enhanced apoptosis was blocked by 2-APB and KN93. Furthermore, HG increased JNK phosphorylation and Fas expression, and both responses were partially blocked by 2-APB and KN93, while the JNK inhibitor SP600125 partially reduced HG-induced Fas expression. In addition, HG depolarized the ΔΨm and triggered the release of mitochondrial cytochrome c. These early signs of mitochondria-dependent apoptosis were partially reversed by 2-APB and KN93. HG-induced apoptosis in RF/6A cells depends on Ca(2+) entry and CaMKII activation, leading to the activation of both Fas-dependent and mitochondria-dependent apoptosis pathways. The CaMKII-JNK-Fas pathway is involved in HG-evoked apoptosis of RECs.
    Molecular vision 09/2012; 18:2371-9. · 2.25 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Necroptosis is a recently discovered programmed necrosis. Evidence demonstrated the importance of necroptosis in neuronal cell death. Necrostatin-1 is a specific inhibitor of necroptosis. In this study, we investigated the role of necrostatin-1 on photoreceptor survival and functional protection after experimental retinal detachment (RD) in rats. Necrostatin-1/inactive analogue of necrostatin-1 was introduced into the subretinal space at RD induction and 6 hours afterward, respectively. We found that necrostatin-1 attenuated retinal histopathological damage and reduced plasma membrane breakdown (a morphological hallmark of necroptosis) in outer retinal layers. Transmission electron microscopy showed that necrostatin-1 directly protected neurons by inhibiting necroptotic, not apoptotic, cell death. Treatment with necrostatin-1 inhibited the induction of receptor-interacting protein kinase phosphorylation after RD (a biomarker of necroptosis). Finally, electroretinographic recording proved that necrostatin-1 contributed to objective functional improvement after RD. These findings indicate that necrostatin-1 is a promising therapeutic agent that protects photoreceptors from necroptosis and improves functional outcome.
    American Journal Of Pathology 08/2012; 181(5):1634-41. DOI:10.1016/j.ajpath.2012.07.029 · 4.60 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: To investigate the effects of high glucose (HG) medium on expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) in cultured rat retinal Müller cells and to determine the signaling pathways mediating the effects. Primary cultures of retinal Müller cells were prepared from Sprague-Dawley rats, and incubated in a medium containg HG (30 mmol/L) in the presence of the membrane-permeable Ca(2+) chelator BAPTA-AM (10 μmol/L) or the CaMKII inhibitor KN93 (10 μmol/L). The levels of CaMKII, p-CaMKII, CREB, p-CREB, HIF-1α, and VEGF proteins were measured with Western blotting, while HIF-1á and VEGF mRNA levels were determined using real-time RT-PCR. The stimulation of retinal Müller cell with HG for 24 h remarkably increased the expression levels of HIF-1α and VEGF. These responses were significantly inhibited in the presence of BAPTA-AM or KN93. Both BAPTA-AM and KN93 also significantly inhibited HG-induced phosphorylation of CaMKII and CREB in the cultured retinal Müller cells. Transfection of the cultured retinal Müller cells with antisense CREB oligonucleotide (300 nmol/L) was similarly effective in blocking the HG-induced increase of HIF-1α and VEGF. HG-induced HIF-1α and VEGF expression in cultured rat retinal Müller cells depends on intracellular free Ca(2+) and activation of CaMKII-CREB pathway. The activation of CaMKII-CREB pathway by HG may be a possible mechanism underlying the pathogenesis of diabetic retinopathy.
    Acta Pharmacologica Sinica 07/2012; 33(8):1030-6. DOI:10.1038/aps.2012.61 · 2.50 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: To test the hypothesis that a microalbuminuria (MA) threshold can help predict the risk for the development of diabetic retinopathy (DR) in type 2 diabetes mellitus (T2DM)_ patients. We conducted a cross-sectional study of 4739 subjects with T2DM and a prospective study of 297 subjects with T2DM in China respectively. Clinical and laboratory data were collected and biologic risk factors associated with any DR were analysed. In the cross-sectional study, we found that MA was an independent risk factor for DR development; further, when the patients were divided into MA deciles, odds ratio (ORs) of DR for the patients in the sixth MA decile (10.7 mg/24 h) was 1.579-fold (1.161-2.147) compared to that for patients in the first MA decile. Furthermore, the OR of DR increased with a gradual increase in MA levels. Similarly, in the prospective study, during a mean follow-up of 4.5 years, we found that 51 patients (29.0%) of the 176 subjects with high MA level (10.7-30 mg/24 h) developed DR, while 17 patients (14.1%) of the 121 subjects with lower MA (<10.7 mg/24 h) developed DR, and the relative risk ratio of the development of DR is 2.13(95% CI, 1.58-3.62, P<0.001). These data suggest that an MA threshold can predict the risk for the development of DR in type 2 diabetes mellitus, although it is still within the traditionally established normal range.
    PLoS ONE 05/2012; 7(5):e36718. DOI:10.1371/journal.pone.0036718 · 3.53 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aims: To assess the association between the NOS3 4b/a, T-786C and G894T polymorphisms and diabetic retinopathy (DR) susceptibility. Materials and Methods: Twenty-one studies covering 8,111 subjects were included. The fixed or random effect model used was based on heterogeneity. Results: A significant association of the intron 4a allele in the NOS3 4b/a polymorphism with reduced risk of DR was found in dominant (OR 0.778, 95% CI 0.654-0.926) and additive (OR 0.809, 95% CI 0.698-0.937) models. Subgroup analysis revealed that the intron 4a allele additive model (OR 0.807, 95% CI 0.697-0.935) was associated with DR risk in type 2 diabetic patients. We also found a marginally significant association of the C allele in the T-786C polymorphism with reduced risk of proliferative DR. In contrast, no statistically significant association was observed between the G894T polymorphism and DR risk, either in the overall or subgroup analyses. Conclusions: The intron 4a allele of the 4b/a polymorphism in the eNOS gene has protective effects against DR, especially in type 2 diabetic patients. The C allele of the T-786C polymorphism may be a protective factor for proliferative DR. However, the G894T polymorphism does not appear to influence the development of DR. This conclusion warrants confirmation by further studies.
    Ophthalmic Genetics 04/2012; 33(4):200-7. DOI:10.3109/13816810.2012.675398 · 1.23 Impact Factor
  • Ning Wang, Zhi Zheng, Hui-Yi Jin, Xun Xu
    [Show abstract] [Hide abstract]
    ABSTRACT: Diabetic retinopathy (DR) is one of the most common complications of diabetes. Angiotensin-converting enzyme inhibitor is thought to play an important role in preventing and treating retinal diseases in animal models of DR. The aim of the present study was to investigate the role of angiotensin-converting enzyme inhibitor (ACEI, captopril) in the treatment of patients with non-proliferative DR. Three hundred and seventeen type 2 diabetic patients (88.05% of participants) without or with mild to moderate non-proliferative retinopathy were randomly divided into captopril group (n = 202) and placebo group (n = 115). All subjects received 24-month follow-up. General clinical examinations, including blood pressure and glycated hemoglobin, as well as comprehensive standardized ophthalmic examinations were performed. Color fundus photography and optical coherence tomography (OCT) were used to grade diabetic retinopathy and detect macular edema respectively. The levels of blood pressure and glycated hemoglobin in the two groups of patients remained within the normal range during the entire follow-up and no significant difference was found between the initial and last visits, suggesting that ACEI drugs play a protective role on the DR patients independent of its anti-blood pressure role. DR classification showed that 169 eyes (83.66%) remained unchanged and the DR grade of 33 eyes (16.34%) increased in captopril group, while 84 eyes (73.04%) remained unchanged and the grade of 31 eyes (26.96%) increased in placebo group (P = 0.024). Captopril treatment improved macular edema in 55.45% eyes, which was significantly higher than the 37.39% improvement in placebo group (P = 0.002). No significant difference was found in the visual acuity between the two groups (P = 0.271). Captopril can improve or delay the development of DR and macular edema, which can be used in the early treatment of DR patients with type 2 diabetic mellitus.
    Chinese medical journal 01/2012; 125(2):287-92. DOI:10.3760/cma.j.issn.0366-6999.2012.02.023 · 1.02 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Focal organizing pneumonia is a unique form of organizing pneumonia. Little is known regarding its clinical and radiological feature, diagnosis, management, and outcome. Twenty patients with focal organizing pneumonia were investigated and compared with 40 patients with bronchogenic carcinoma. There were 38 men (63.3%) and 22 women (36.7%). The mean age was 55 ± 9.9 years. No specific feature in clinical and radiological manifestation was found to distinguish between focal organizing pneumonia and bronchogenic carcinoma. In patients with focal organizing pneumonia, wedge resection was performed in 12 cases and lobectomy in eight cases. Follow-up was complete with a median period of 26 months (range, 6 to 104 months). All patients were free from recurrence of organizing pneumonia. Clinical and radiologic findings of focal organizing pneumonia are nonspecific, and this unique form of organizing pneumonia is difficult to differentiate from lung cancer. Surgical resection allows both diagnosis and cure. However, considering the benign nature of this disease, major pulmonary resections should be avoided.
    The American surgeon 01/2012; 78(1):133-7. · 0.92 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Cellular metabolic memory occurs in diabetic microvascular and macrovascular complications, but the underlying mechanisms remain unclear. Here, we investigate the role of sirtuin 1 (SIRT1) and metformin in this phenomenon. In bovine retinal capillary endothelial cells (BRECs) and retinas of diabetic rats, the inflammatory gene, nuclear factor-κB (NF-κB), and the proapoptotic gene, Bax, induced by hyperglycemia, remained elevated after returning to normoglycemia. BRECs with small interfering RNA-mediated SIRT1 knockdown had increased sensitivity to hyperglycemia stress, whereas SIRT1 overexpression or activation by metformin inhibited the increase of mitochondrial reactive oxygen species-mediated glyceraldehyde-3-phosphate dehydrogenase by poly (ADP-ribose) polymerase (PARP) activity through the upregulation of liver kinase B1/AMP-activated protein kinase (LKB1/AMPK), ultimately suppressing NF-κB and Bax expression. Furthermore, we showed that hyperglycemia led to PARP activation, which in turn may have downregulated SIRT1. Of importance, this study also demonstrated that metformin suppressed the "memory" of hyperglycemia stress in the diabetic retinas, which may be involved in the SIRT1/LKB1/AMPK pathway. Our data suggest that SIRT1 is a potential therapeutic target for the treatment of the cellular metabolic memory, and the use of metformin specifically for such therapy may be a new avenue of investigation in the diabetes field.
    Diabetes 11/2011; 61(1):217-28. DOI:10.2337/db11-0416 · 8.47 Impact Factor

Publication Stats

143 Citations
73.56 Total Impact Points

Institutions

  • 2014
    • Hangzhou First People's Hospital
      Hang-hsien, Zhejiang Sheng, China
  • 2013–2014
    • Peking Union Medical College Hospital
      Peping, Beijing, China
    • Chinese Academy of Medical Sciences
      Peping, Beijing, China
  • 2012–2014
    • Shanghai Putuo District People's Hospital
      Shanghai, Shanghai Shi, China
    • Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine
      Shanghai, Shanghai Shi, China
  • 2011–2014
    • Shanghai Jiao Tong University
      • Department of Ophthalmology
      Shanghai, Shanghai Shi, China
    • Shanghai University
      • Department of Ophthalmology
      Shanghai, Shanghai Shi, China
  • 2004–2012
    • Tongji Hospital
      Wu-han-shih, Hubei, China
  • 2005–2011
    • Huazhong University of Science and Technology
      • Department of Cardio Thoracic Surgery
      Wu-han-shih, Hubei, China