Effect of sodium hyaluronate in treating fungal corneal ulcer

AIM: To retrospectively analyze the effects of sodium hyaluronate in treating fungal corneal ulcer.<p>METHODS: Since June, 2006, there were 178 patients(178 eyes)with fungal corneal ulcer receiving medical treatment in our hospital. Among them, 81 patients(81 eyes)as the control group received the traditional antifungal treatment with the natamycin and fluconazole being the major medicine, from June 2006 to June 2008. While, 97 patients(97 eyes)as the treatment group received sodium hyaluronate treatment based on traditional antifungal treatment during the period of June 2008 to March 2010. Effects of two therapeutic methods were compared and analyzed. <p>RESULTS: Of the 97 cases in the treatment group, the average hospital stay was: 14.15±4.23d, with 90 cases(92.8%)cured, 5 cases(5.2%)improved, 2 cases(2.1%)ineffective, the final visual acuity of 51.6% patients better than 0.3. Of the 81 cases in the control group, average hospital stay was: 17.26±6.23d, with 69 cases(85.2%)cured, 7 cases(8.6%)improved, 5 cases(6.2%)ineffective, the final visual acuity of 39.5% patients better than 0.3. After statistical analysis, the average hospital stay, the cure rate, the effective rate and the final visual acuity in both groups showed statistically significant difference(<i>P</i><0.05). The average hospital stay of the treatment group was shorter than that of the control group, while the cure rate and effective rate and the final visual acuity was better than that of the control group.<p>CONCLUSION: Sodium hyaluronate can promote fungal corneal ulcer healing, improve the cure rate and reduce the formation of corneal scar

Effect of Astragalus membranaceus (Fisch) Bunge extract on streptozocin-induced diabetic in rats

Purpose: To investigate the effect of Astragalus membranaceus (Fisch.) Bunge. extract (AMBE) on streptozotocin-induced diabetic rats.Methods: The aqueous extract of AMB was obtained by steeping the dried  Astragalus membranaceus (Fisch.) Bunge. in water at 60 oC three times, each for 1 h, before first drying in an oven at 100 oC and then freeze-drying the last extract thus obtained. Diabete model rats was induced by a single intraperitoneal injection of a freshly prepared solution of streptozotocin (50 mg/kg). The rats were randomly divided into 6 groups of ten rats each: negative control group, normal control group, reference group (glibenclamide1 mg/kgbody weight) as well as AMB extract groups, namely, 40, 80 and 160 mg/kg body weight. Antihyperglycemic effect was measured by blood glucose and plasma insulin levels. Oxidative stress was evaluated in liver and kidney by antioxidant markers, viz, lipidperoxidation (LPO), superoxide  dismutase (SOD), reduced glutathione (GSH), glutathione peroxidase (GPx) and catalase (CAT), while blood serum levels of creatinine and urea were also determined in both diabetic control and treated rats.Results: Compared with diabetic rats, oral administration of AMBE at a  concentration of 160 mg/kg daily for 30 days showed a significant decrease in fasting blood glucose (109.438 ± 3.52, p &lt; 0.05) and increased insulin level (13.96 ± 0.74, p &lt; 0.05). Furthermore, it significantly reduced biochemical parameters (serum creatinine, 0.86 ± 0.29, p &lt; 0.05) and serum urea (45.14 ± 1.79, p &lt; 0.05). The treatment also resulted in significant increase in GSH (49.21 ± 2.59, p &lt; 0.05), GPx (11.96 ± 1.16, p &lt; 0.05), SOD (14.13 ± 0.49, p &lt; 0.05), CAT (83.25 ± 3.14, p &lt; 0.05) level in the liver and kidney of diabetic rats.Conclusion: The results suggest that AMBE may effectively normalize impaired  antioxidant status in streptozotocin-induced diabetes in a dose-dependent manner. AMBE has a protective effect against lipid peroxidation by scavenging free radicals and is thus capable of reducing the risk of diabetic complications.Keywords: Astragalus membranaceus, Diabetic, Antihyperglycemic, Antioxidant Oxidative stress, Fasting blood glucos

Reinforcement Learning Approaches for Traffic Signal Control under Missing Data

The emergence of reinforcement learning (RL) methods in traffic signal control tasks has achieved better performance than conventional rule-based approaches. Most RL approaches require the observation of the environment for the agent to decide which action is optimal for a long-term reward. However, in real-world urban scenarios, missing observation of traffic states may frequently occur due to the lack of sensors, which makes existing RL methods inapplicable on road networks with missing observation. In this work, we aim to control the traffic signals in a real-world setting, where some of the intersections in the road network are not installed with sensors and thus with no direct observations around them. To the best of our knowledge, we are the first to use RL methods to tackle the traffic signal control problem in this real-world setting. Specifically, we propose two solutions: the first one imputes the traffic states to enable adaptive control, and the second one imputes both states and rewards to enable adaptive control and the training of RL agents. Through extensive experiments on both synthetic and real-world road network traffic, we reveal that our method outperforms conventional approaches and performs consistently with different missing rates. We also provide further investigations on how missing data influences the performance of our model.Comment: Published as a conference paper at IJCAI202

Depletion of OLFM4 gene inhibits cell growth and increases sensitization to hydrogen peroxide and tumor necrosis factor-alpha induced-apoptosis in gastric cancer cells

<p>Abstract</p> <p>Background</p> <p>Human olfactomedin 4 (OLFM4) gene is a secreted glycoprotein more commonly known as the anti-apoptotic molecule GW112. OLFM4 is found to be frequently up-regulated in many types of human tumors including gastric cancer and it was believed to play significant role in the progression of gastric cancer. Although the function of OLFM4 has been indicated in many studies, recent evidence strongly suggests a cell or tissue type-dependent role of OLFM4 in cell growth and apoptosis. The aim of this study is to examine the role of gastric cancer-specific expression of OLFM4 in cell growth and apoptosis resistance.</p> <p>Methods</p> <p>OLFM4 expression was eliminated by RNA interference in SGC-7901 and MKN45 cells. Cell proliferation, anchorage-independent growth, cell cycle and apoptosis were characterized in vitro. Tumorigenicity was analyzed in vivo. The apoptosis and caspase-3 activation in response to hydrogen peroxide (H₂O₂) or tumor necrosis factor-alpha (TNF α) were assessed in the presence or absence of caspase inhibitor Z-VAD-fmk.</p> <p>Results</p> <p>The elimination of OLFM4 protein by RNA interference in SGC-7901 and MKN45 cells significantly inhibits tumorigenicity both in vitro and in vivo by induction of cell G1 arrest (all P < 0.01). OLFM4 knockdown did not trigger obvious cell apoptosis but increased H₂O₂or TNF α-induced apoptosis and caspase-3 activity (all P < 0.01). Treatment of Z-VAD-fmk attenuated caspase-3 activity and significantly reversed the H₂O₂or TNF α-induced apoptosis in OLFM4 knockdown cells (all P < 0.01).</p> <p>Conclusion</p> <p>Our study suggests that depletion of OLFM4 significantly inhibits tumorigenicity of the gastric cancer SGC-7901 and MKN45 cells. Blocking OLFM4 expression can sensitize gastric cancer cells to H₂O₂or TNF α treatment by increasing caspase-3 dependent apoptosis. A combination strategy based on OLFM4 inhibition and anticancer drugs treatment may provide therapeutic potential in gastric cancer intervention.</p