Low Au-content CoAu electrodes for environmental applications

Six cobalt gold (CoAu) electrodes were prepared by electroless deposition using different gold-containing solutions (acidic and weakly acidic) and different Au deposition times. Characterization of CoAu electrodes was done by scanning electron microscopy with energy-dispersive X-ray spectroscopy, N₂-sorption, and X-ray powder diffraction techniques. The possibility of using the prepared electrodes in environmental applications, i.e., for the electrochemical sensing of a trace amount of arsenic(iii) in weakly alkaline media was assessed. Employing the CoAu electrode (prepared by immersing Co/Cu into 1 mM HAuCl₄ (pH 1.8) at 30 °C for 30 s) under optimized conditions (deposition potential −0.7 V and deposition time of 60 s), a low limit of detection of 2.16 ppb was obtained. Finally, this CoAu electrode showed activity for arsenic oxidation in the presence of Cu(ii) as a model interferent as well as in real samples. Furthermore, the use of CoAu electrode as an anode in fuel cells, namely, direct borohydride – hydrogen peroxide fuel cells was also assessed. A peak power density of 191 mW cm⁻² was attained at 25 °C for DBHPFC with CoAu anode at a current density of 201 mA cm⁻² and cell voltage of 0.95 V, respectively. The peak power density further increased with the increase of the operating temperature to 55 °C.

A low Au-content CoAu electrode prepared by simple electroless deposition outperforms a pure Au electrode for versatile environmental applications: As(iii) sensing in water or as electrodes in direct borohydride-hydrogen peroxide fuel cells.     

Induction of kinetochore-containing micronuclei by exogenous 06-methylguanine requires conversion of the methylated base to a nucleotide

It has been reported that exogenous alkylated purines, such as O6-methylguanine (O6meG), induce aneuploidy in mammalian cells. It is shown here that the aneugenic effect of O6meG, evidenced by its ability to induce micronuclei in rodent cells, is dependent on its conversion to O6-methyl-guano-sine-5′-monophosphate (O6me-5′-GMP) by hypo-xanthine-guanine phosphoribosyl transferase (HPRT). This conclusion, in contrast with previous in vitro data showing that O6meG does not seem to be a substrate for HPRT, was based on the following observations: 1) O6meG did not induce micronuclei in HPRT-deficient Chinese hamster cells, but did induce micronuclei in HPRT-proficient cells, and in mouse cells partially or totally deficient in adenine phosphoribosyl transferase; 2) O6meG was not metabolized in HPRT-deficient cells, while in wild-type cells a number of metabolites were detected by high performance liquid chromatography (HPLC) analysis of cold acid extracts, one of them coeluting with O6me-5′-GMP used as a marker; 3) when de novo synthesis of purine nucleotides was inhibited by aminopterin, O6meG sustained the growth of HPRT-proficient, but not of HPRT-deficient, cells; and 4) when HPRT-deficient cells were treated with lipo-somes charged with O6me-5′-GMP, induction of micronuclei was shown. The finding that methylated guanine exerts its aneugenic action through methylated nucleotide(s) provides an important, though indirect, support to the hypothesis that alkylating agents may induce aneuploidy via nucleotide pool alkylation. © 1995 Wiley-Liss, Inc.     

Short-lived effect of (des-tyr)-gamma-endorphin in schizophrenia

Des-tyrosine-γ-endorphin (DTγE) has been reported to alleviate symptoms of schizophrenia. Attempting to replicate those reports, we administered 1 mg of DTγE, i.m., for 8 consecutive days to nine patients meeting the DSM-III criteria for schizophrenia. Patients in this double-blind, crossover, and placebo-controlled study showed a statistically significant, but clinically modest improvement. The improvement was detectable during the first several days of the DTγE treatment; the symptoms then returned to baseline level in spite of continued doses of DTγE. Testing the metabolism of DTγE in the patients' plasma, we found a high rate of formation and of degradation, but the metabolic rates were not related to clinical symptoms.     

A dry mouth and oedematous ankle.

A 59-year-old woman, suffering from primary Sjögren's syndrome(pSS) since the age of 48, was treated symptomatically. In 2003a marginal zone B-cell lymphoma was diagnosed, localized inthe mediastinum, producing IgM paraproteins. This type of lymphomais a low grade lymphoma and observation without treatment islegitimate. In August 2004 she experienced ankle oedema and foamy urine.Physical examination revealed hypertension (170/95 mmHg) andperipheral leg oedema. Laboratory data showed: haemoglobin 7.3mmol/l, white cell count 7.3x10⁹/l, thrombocytes 603x10⁹/l,serum sodium 133 mmol/l, potassium 4.6 mmol/l, serum     

Phytoecdysteroids--from isolation to their effects on humans

An overview is given on both well-known and recently discovered phytoecdyteroids including a sophisticated isolation scheme and notable physiological and pharmacological effects of ecdysteroids on vertebrates. The isolation of pure ecdysteroids has been improved by the use of low-pressure reversed-phase chromatography. An optimized combination of preliminary purification and chromatographic separations results in pure ecdysteroids. Structural elucidation has been done using spectroscopic methods, however, the final proof of the steric structure is rendered using x-ray crystallography. Ecdysteroid containing preparations show a boom and both OTC products and numerous preparation techniques can be found using the Internet. This paper will give a review on the kaleidoscope of pharmacological effects attributed to the ecdysteroids, such as: An increase of protein synthesis (for body-building, AIDS, patients with neoplasm disease, etc.), and other body functions; Antidepressant effect; Shielding the body from stress, and improve the physical and sexual performance; Prevention from infections and certain diseases. A list of recent offers of ecdysteroid-containing products will also be given. The perspective use of ecdysteroids is promising in genetics. Steroid regulation of programmed cell death during development and differentiation has recently come to the limelight. Murine model of human diseases and its influencing with ecdysteroids are detailed.     

Mucopolysaccharidosis type II in females and response to enzyme replacement therapy

Mucopolysaccharidosis type II (MPS II, Hunter syndrome) is an X-linked lysosomal storage disease caused by a deficiency of iduronate-2-sulfatase (IDS). Two affected girls with moderate and severe forms of MPS II with normal karyotypes and increased urinary dermatan sulphate and heparin sulphate excretion and marked deficiencies of IDS activity are reported. Molecular studies showed that case 1 has a heterozygous mutation c.1568A?>?G (p.Y523C) associated with almost totally skewed inactivation of the normal maternal X chromosome, and case 2 has a heterozygous deletion that includes exons 1-4 of IDS (minimal deletion range c.1-103_184del). The multi-exon deletion correlated with early onset of the disease and severe phenotype with intellectual disability, whereas the missense mutation was associated with moderate developmental delay. Although genotype-phenotype correlation in MPS II is difficult, gene deletions seem to correlate with more severe clinical manifestation of the disease. Enzyme replacement therapy (ERT) in these two females resulted in disease stabilization in both.     

Protein kinase inhibitor as a potential candidate for epilepsy treatment

Purpose: Effects of the “VID‐82925” kinase inhibitor molecule were investigated both during the developing phase as well as during the stable phase of the focus with spontaneous recurrent seizures using the 4‐AP‐induced in vivo epilepsy model in anesthetized rats. Methods: In electrophysiologic experiments, VID‐82925 (0.85 mg/kg) was injected intravenously either before the induction (pretreatment) or after the development of the stable focus (treatment). Reference drugs carbamazepine (4.8 mg/kg) and levetiracetam (50 mg/kg) were employed using the same experimental paradigm. The antiepileptic effect of VID‐82925 was also compared to those of the broad‐spectrum gap junction channel blocker carbenoxolone (10 mm ). Key Findings: Pretreatment with VID‐82925 revealed an antiepileptogenic effect as it suppressed significantly the manifestation of the epileptiform activity not only during the developing phase, but also for a considerable long period during the stable phase of the focus. The current data do not allow us to differentiate an antiictal treatment effect from an antiepileptogenic effect of the compound during the stable phase of the focus. Treatment with VID‐82925 was also effective against ictogenesis during the stable phase of the focus. Pretreatment with levetiracetam failed to exert any antiepileptogenic effect. The antiepileptic effects of VID‐82925 and of the reference drugs on the epileptiform activity of the stable focus were comparable in intensity; however, the effect of VID‐82925 was 2–3 times longer. The effects of VID‐82925 and of carbenoxolone overlapped one another to some extent, suggesting that VID‐82925 may exert its effects at least partially through blocking of gap junctional communication. Significance: Our results indicate that inhibition of protein kinases may also provide an effective strategy for the development of a drug that is not only antiepileptic but also depresses the course of epileptogenesis.