Discussion on the Relevance of Old Low-lying Land Reclamation and Soil Liquefaction

Source: ICHE Conference Archive - https://mdi-de.baw.de/icheArchive

A Simple Model for Cavity Enhanced Slow Lights in Vertical Cavity Surface Emission Lasers

We develop a simple model for the slow lights in Vertical Cavity Surface Emission Lasers (VCSELs), with the combination of cavity and population pulsation effects. The dependences of probe signal power, injection bias current and wavelength detuning for the group delays are demonstrated numerically and experimentally. Up to 65 ps group delays and up to 10 GHz modulation frequency can be achieved in the room temperature at the wavelength of 1.3 $\mu$m. The most significant feature of our VCSEL device is that the length of active region is only several $\mu$m long. Based on the experimental parameters of quantum dot VCSEL structures, we show that the resonance effect of laser cavity plays a significant role to enhance the group delays

Attenuation of Brain Nitrostative and Oxidative Damage by Brain Cooling during Experimental Traumatic Brain Injury

The aim of the present study was to ascertain whether brain cooling causes attenuation of traumatic brain injury by reducing brain nitrostative and oxidative damage. Brain cooling was accomplished by infusion of 5 mL of 4°C saline over 5 minutes via the external jugular vein. Immediately after the onset of traumatic brain injury, rats were randomized into two groups and given 37°C or 4°C normal saline. Another group of rats were used as sham operated controls. Behavioral and biochemical assessments were conducted on 72 hours after brain injury or sham operation. As compared to those of the sham-operated controls, the 37°C saline-treated brain injured animals displayed motor deficits, higher cerebral contusion volume and incidence, higher oxidative damage (e.g., lower values of cerebral superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, but higher values of cerebral malondialdehyde), and higher nitrostative damage (e.g., higher values of neuronal nitric oxide synthase and 3-nitrotyrosine). All the motor deficits and brain nitrostative and oxidative damage were significantly reduced by retrograde perfusion of 4°C saline via the jugular vein. Our data suggest that brain cooling may improve the outcomes of traumatic brain injury in rats by reducing brain nitrostative and oxidative damage

The p53-dependent apoptotic pathway of breast cancer cells (BC-M1) induced by the bis-type bioreductive compound aziridinylnaphthoquinone

INTRODUCTION: Several aziridinylbenzoquinone drugs have undergone clinical trials as potential antitumor drugs. These bioreductive compounds are designed to kill cells preferentially within the hypoxia tumor microenvironment. The bioreductive compound of bis-type naphthoquinone synthesized in our laboratory, 2-aziridin-1-yl-3-[(2-{2-[(3-aziridin-1-yl-1,4-dioxo-1,4-dihydronaphthalen-2-yl)thio]ethoxy}ethyl)thio]naphthoquinone (AZ-1), had the most potent death effect on the breast cancer cells BC-M1 in our previous screening. In the present study, we determined that the mechanism of the death effect of BC-M1 cells induced by AZ-1 was mediated by the apoptosis pathway. METHODS: We evaluated the cytotoxicity of AZ-1 and the anti-breast cancer drugs tamoxifen and paclitaxel to BC-M1 cells and MCF-7 cells by the MTT assay and measured the apoptosis phenomena by Hoechst 33258 staining for apoptotic bodies. We also quantified the sub-G(1 )peak area and the ratio of the CH(2)/CH(3 )peak area of the cell membrane in BC-M1 cells by flow cytometry and (1)H-NMR spectra, respectively. The apoptosis-related protein expressions, including p53, p21, the RNA-relating protein T-cell restricted intracellular antigen-related protein, cyclin-dependent kinase 2 (cell cycle regulating kinase) and pro-caspase 3, were detected by western blot, and the caspase-3 enzyme activity was also quantified by an assay kit. RESULTS: AZ-1 induced two of the breast cancer cell lines, with IC(50 )= 0.51 μM in BC-M1 cells and with IC(50)= 0.57 μM in MCF-7 cells, and showed less cytotoxicity to normal fibroblast cells (skin fibroblasts) with IC(50)= 5.6 μM. There was a 10-fold difference between two breast cancer cell lines and normal fibroblasts. Of the two anti-breast cancer drugs, tamoxifen showed IC(50)= 0.12 μM to BC-M1 cells and paclitaxel had much less sensitivity than AZ-1. The expression of p53 protein increased from 0.5 to 1.0 μM AZ-1 and decreased at 2.0 μM AZ-1. The p21 protein increased from 0.5 μM AZ-1, with the highest at 2 μM AZ-1. Regarding the AZ-1 compound-induced BC-M1 cells mediating the apoptosis pathway, the apoptotic body formation, the sub-G(1 )peak area, the ratio of CH(2)/CH(3 )of phospholipids in the cell membrane and the enzyme activity of caspase-3 were all in direct proportion with the dose-dependent increase of the concentration of AZ-1. The death effect-related proteins, including T-cell restricted intracellular antigen-related protein, cyclin-dependent kinase 2, and pro-caspase-3, all dose-dependently decreased with AZ-1 concentration. CONCLUSIONS: The AZ-1-induced cell death of BC-M1 cells mediating the apoptosis pathway might be associated with p53 protein expression, and AZ-1 could have the chance to be a candidate drug for anti-breast cancer following more experimental evidence, such as animal models

Enhanced Antifungal Bioactivity of Coptis Rhizome Prepared by Ultrafining Technology

The aim of this study was to identify and quantify the bioactive constituents in the methanol extracts of Coptis Rhizome prepared by ultrafining technology. The indicator compound was identified by spectroscopic method and its purity was determined by HPLC. Moreover, the crude extracts and indicator compound were examined for their ability to inhibit the growth of Rhizoctonia solani Kühn AG-4 on potato dextrose agar plates. The indicator compound is a potential candidate as a new plant derived pesticide to control Rhizoctonia damping-off in vegetable seedlings. In addition, the extracts of Coptis Rhizome prepared by ultrafining technology displayed higher contents of indicator compound; they not only improve their bioactivity but also reduce the amount of the pharmaceuticals required and, thereby, decrease the environmental degradation associated with the harvesting of the raw products

Predictors of intra-abdominal coagulopathic hemorrhage after living donor liver transplantation

AbstractBackgroundResults of preoperative conventional coagulation assays are a poor predictor of hemorrhage after liver transplantation. In this study, we evaluated the factors that are predictive of intra-abdominal coagulopathic hemorrhage after living donor liver transplantation surgery.MethodsDuring the period from January 2009 to December 2012, 118 adults underwent living donor liver transplantation (LDLT) in our institution. Of those patients, 18 (15.3%) developed intra-abdominal coagulopathic hemorrhage (n = 7) or hemorrhage due to non-coagulopathic causes (n = 11) that required emergency medical, radiological, or surgical intervention within the first month after LDLT. Possible predictors of postoperative coagulopathic hemorrhage included donor-related factors, age, body mass index, MELD score, INR value, intra-operative blood transfusion, graft/recipient weight ratio, anhepatic phase, cold ischemia time, operative time, APACHE II score, onset of re-bleeding, and hemoglobin levels during rebleeding episodes.ResultsThere were no differences in any of the variables between the two groups (coagulopathic and noncoagulopathic hemorrhage) except for cold ischemia time. We found that cold ischemia time was significantly longer in patients with postoperative coagulopathic hemorrhage (160.50 ± 45.02 min) than in patients with hemorrhage due to non-coagulopathic causes (113.55 ± 29.31 min; P = 0.027).ConclusionProlonged cold ischemia time is associated with postoperative intra-abdominal coagulopathic hemorrhage in patients after LDLT. It is, therefore, necessary to shorten the cold ischemia time in order to reduce the risk of postoperative intra-abdominal hemorrhage due to coagulopathic causes