Influence of Mixed Solvent on the Electrochemical Property of Hybrid Capacitor.

The hybrid capacitors (2245 size, cylindrical type) were prepared by using activated carbon cathode and Li4Ti5O12 anode. In order to improve the cell operation at high temperature range, propylene carbonate (PC) was used in combination with acetonitrile (AN) with volume ratio of 7:3, 5:5, and 3:7, respectively. We investigated the electrochemical behavior of the hybrid capacitors that enabled cell operation with stability at high temperature. The organic electrolyte of hybrid capacitor containing PC and AN with a volume ratio 7:3 intended to exhibit highly reversible cycle performance with good capacity retention at 60 degrees C after 2200 cycles. From this study, it has been found that the very strong influence of the solvent nature on the characteristics of hybrid capacitor, and the difference in performance associated with the two solvents.

Loss of PTEN induces microtentacles through PI3K-independent activation of cofilin.

Loss of PTEN tumor suppressor enhances metastatic risk in breast cancer, although the underlying mechanisms are poorly defined. We report that homozygous deletion of PTEN in mammary epithelial cells induces tubulin-based microtentacles (McTNs) that facilitate cell reattachment and homotypic aggregation. Treatment with contractility-modulating drugs showed that McTNs in PTEN(-/-) cells are suppressible by controlling the actin cytoskeleton. Because outward microtubule extension is counteracted by actin cortical contraction, increased activity of actin-severing proteins could release constraints on McTN formation in PTEN(-/-) cells. One such actin-severing protein, cofilin, is activated in detached PTEN(-/-) cells that could weaken the actin cortex to promote McTNs. Expression of wild-type cofilin, an activated mutant (S3A), and an inactive mutant (S3E) demonstrated that altering cofilin phosphorylation directly affects McTNs formation. Chemical inhibition of PI3K did not reduce McTNs or inactivate cofilin in PTEN(-/-) cells. Additionally, knock-in expression of the two most common PI3K-activating mutations observed in human cancer patients did not increase McTNs or activate cofilin. PTEN loss and PI3K activation also caused differential activation of the cofilin regulators, LIM-kinase1 (LIMK) and Slingshot-1L (SSH). Furthermore, McTNs were suppressed and cofilin was inactivated by restoration of PTEN in the PTEN(-/-) cells, indicating that both the elevation of McTNs and the activation of cofilin are specific results arising from PTEN loss. These data identify a novel mechanism by which PTEN loss could remodel the cortical actin network to facilitate McTNs that promote tumor cell reattachment and aggregation. Using isogenic MCF-10A PTEN(-/-) and PIK3CA mutants, we have further demonstrated that there are clear differences in activation of cofilin, LIMK and SSH between PTEN loss and PI3K activation, providing a new evidence that these mutations yield distinct cytoskeletal phenotypes, which could have an impact on tumor biology.

Comparison of the predictive power of the LODS and APACHE II scoring systems in a neurological intensive care unit.

OBJECTIVE: A prospective study to compare the power of the Logistic Organ Dysfunction System (LODS) and the Acute Physiology and Chronic Health Evaluation II (APACHE II) scoring systems to predict survival, in patients admitted to the neurological intensive care unit (NICU). METHODS: Clinical data from 521 consecutive NICU patients were collected during the first 24 h of admission and were used to compare the predictive power of both scoring systems. RESULTS: The observed mortality rate was 10.0% compared with predicted mortality rates of 7.2% and 4.8% according to LODS and APACHE II, respectively. Both scoring systems had excellent discrimination but LODS had superior calibration. CONCLUSION: The LODS scoring system was more stable than the APACHE II scoring system in the NICU setting.

Metastatic breast tumors express increased tau, which promotes microtentacle formation and the reattachment of detached breast tumor cells.

The cytoskeletal organization of detached and circulating tumor cells (CTCs) is currently not well defined and may provide potential targets for new therapies to limit metastatic tumor spread. In vivo, CTCs reattach in distant tissues by a mechanism that is tubulin-dependent and suppressed by polymerized actin. The cytoskeletal mechanisms that promote reattachment of CTCs match exactly with the mechanisms supporting tubulin microtentacles (McTN), which we have recently identified in detached breast tumor cells. In this study, we aimed to investigate how McTN formation is affected by the microtubule-associated protein, tau, which is expressed in a subset of chemotherapy-resistant breast cancers. We demonstrate that endogenous tau protein localizes to McTNs and is both necessary and sufficient to promote McTN extension in detached breast tumor cells. Tau-induced McTNs increase reattachment of suspended cells and retention of CTCs in lung capillaries. Analysis of patient-matched primary and metastatic tumors reveals that 52% possess tau expression in metastases and 26% display significantly increased tau expression over disease progression. Tau enrichment in metastatic tumors and the ability of tau to promote tumor cell reattachment through McTN formation support a model in which tau-induced microtubule stabilization provides a selective advantage during tumor metastasis.

The analgesic effect of remifentanil on prevention of withdrawal response associated with the injection of rocuronium in children: no evidence for a peripheral action.

Remifentanil pre-treatment has been reported to decrease the incidence of rocuronium injection-associated withdrawal movement. This study was designed to explore the site of action of remifentanil for reducing withdrawal response during rocuronium injection in children. Ninety-six paediatric patients were randomly assigned to three groups. After induction of anaesthesia with 5 mg/kg 2.5% thiopental sodium, 2 ml saline (placebo group) or 0.5 microg/kg remifentanil (group R), was injected intravenously 1 min before 0.6 mg/kg rocuronium. In a third group (group R'), the venous retention of 0.5 microg/kg remifentanil was maintained for 30 s followed by tourniquet release and injection of 0.6 mg/kg rocuronium. Withdrawal response was graded using a four-point scale. The incidence of withdrawal movement after rocuronium administration was 94%, 22% and 81% in the placebo, R, and R' groups, respectively. This study demonstrated that the pre-treatment effect of remifentanil for reducing rocuronium-associated withdrawal response occurs mainly through a central action.

Express primer tool for high-throughput gene cloning and expression.

High-throughput approaches for gene cloning and expression require the development of new nonstandard tools for molecular biologists and biochemists. We introduce a Web-based tool to design primers specifically for the generation of expression clones for both laboratory-scale and high-throughput projects. The application is designed not only to allow the user complete flexibility to specify primer design parameters but also to minimize the amount of manual intervention needed to generate a large number of primers for the simultaneous amplification of multiple target genes.