Hydrogen thresholds as indicators of dehalorespiration in constructed treatment wetlands

Anaerobic degradation of cis-1,2-dichloroethene (cis-1,2-DCE) and 1,2-dichloroethane (1,2-DCA) was studied in microcosms derived from a laboratory-scale upflow treatment wetland system used to biodegrade chlorinated compounds present in groundwater from a Superfund site. Dechlorination kinetics of cis-1,2-DCE (0.94-1.57 d(-1)) and 1,2-DCA (0.15-0.71 d(-1)) were rapid, and degradation proceeded to completion with ethene or ethane as terminal dechlorination products. Hydrogen concentrations, measured simultaneously during dechlorination, were significantly different for the two compounds, approximately 2.5 nM for cis-1,2-DCE and 38 nM for 1,2-DCA. Methanogenesis proceeded during the degradation of 1,2-DCA when H2 concentrations were high but not during the dechlorination of cis-1,2-DCE when H2 concentrations were below published thresholds for methanogenesis. A 16S rRNA gene-based approach indicates that microorganisms closely related to Dehalococcoides ethenogenes were present and that they were distributed throughout the bottom, middle, and top of the upflow treatment wetland system. These results coupled with consideration of hydrogen thresholds, degradation kinetics, daughter products, and measurements of methanogenesis strongly suggest that halorespirers were responsible for dechlorination of cis-1,2-DCE and that 1,2-DCA dechlorination was co-metabolic, likely mediated by acetogens or methanogens. Rapid dechlorination potential was distributed throughout the wetland bed, both within and below the rhizosphere, indicating that reductive dechlorination pathways can be active in anaerobic environments located in close spatial proximity to aerobic environments and plants in treatment wetland systems.     

High accuracy peak location and amplitude spectral estimation via tuning APES method

In this paper, we introduce a new approach to the method of non-parametric adaptive spectral analysis by using the Amplitude and Phase Estimation (APES) method, and taking into account the small sample errors of the sample covariance matrix. This approach is referred to as Adaptive Tuning Amplitude and Phase Estimation method (ATAPES). The main advantage of the ATAPES algorithm is its elimination of biased estimation exists with APES method, which is a biased peak location and corresponding problem of the biased amplitude estimation. The ATAPES method provides more accurate peak location and amplitude estimation with higher resolution than APES method.     

Specificity of the SH2 domains of SHP-1 in the interaction with the immunoreceptor tyrosine-based inhibitory motif-bearing receptor gp49B

Inhibitory receptors on hemopoietic cells critically regulate cellular function. Despite their expression on a variety of cell types, these inhibitory receptors signal through a common mechanism involving tyrosine phosphorylation of the immunoreceptor tyrosine-based inhibitory motif (ITIM), which engages Src homology 2 (SH2) domain-containing cytoplasmic tyrosine or inositol phosphatases. In this study, we have investigated the proximal signal-transduction pathway of an ITIM-bearing receptor, gp49B, a member of a newly described family of murine NK and mast cell receptors. We demonstrate that the tyrosine residues within the ITIMs are phosphorylated and serve for the association and activation of the cytoplasmic tyrosine phosphatase SHP-1. Furthermore, we demonstrate a physiologic association between gp49B and SHP-1 by coimmunoprecipitation studies from NK cells. To address the mechanism of binding between gp49B and SHP-1, binding studies involving glutathione S-transferase SHP-1 mutants were performed. Utilizing the tandem SH2 domains of SHP-1, we show that either SH2 domain can interact with phosphorylated gp49B. Full-length SHP-1, with an inactivated amino SH2 domain, also retained gp49B binding. However, binding to gp49B was disrupted by inactivation of the carboxyl SH2 domain of full-length SHP-1, suggesting that in the presence of the phosphatase domain, the carboxyl SH2 domain is required for the recruitment of phosphorylated gp49B. Thus, gp49B signaling involves SHP-1, and this association is dependent on tyrosine phosphorylation of the gp49B ITIMs, and an intact SHP-1 carboxyl SH2 domain.     

A quasi-two-dimensional electrochemistry modeling tool for planar solid oxide fuel cell stacks

A quasi-two-dimensional numerical model is presented for the efficient computation of the steady-state current density, species concentration, and temperature distributions in planar solid oxide fuel cell stacks. The model reduction techniques, engineering approximations, and numerical procedures used to simulate the stack physics while maintaining adequate computational speed are discussed. The results of the model for benchmark cases with and without on-cell methane reformation are presented with comparisons to results from other research described in the literature. Simulations results for a multi-cell stack have also been demonstrated to show capability of the model on simulating cell to cell variation. The capabilities, performance, and scalability of the model for the study of large multi-cell stacks are then demonstrated.     

Conformational state-dependent effects of halothane on cardiac Na+ current

BACKGROUND: The Na+ channel is voltage gated and characterized by three distinct states: closed, open, and inactivated. To identify the effects of halothane on the cardiac Na+ current (I(Na)) at various membrane potentials, the effects of 1.2 mM halothane at different holding potentials (V(H)) on I(Na) were examined in single, enzymatically isolated guinea pig ventricular myocytes. METHODS: The I(Na) was recorded using the whole-cell configuration of the patch-clamp technique. Currents were generated from resting V(H)s of -110, -80, or -65 mV. State-dependent block was characterized by monitoring frequency dependence, tonic block, and removal of inactivation by veratridine. RESULTS: Halothane produced significant (P < 0.05) V(H)-dependent depressions of peak I(Na) (mean +/- SEM): 24.4 +/- 4.1% (V(H) = -110 mV), 42.1 +/- 3.4% (V(H) = -80 mV), and 75.2 +/- 1.5% (V(H) = -65 mV). Recovery from inactivation was significantly increased when cells were held at -80 mV (control, tau = 6.0 +/- 0.3 ms; halothane, tau = 7.1 +/- 0.4 ms), but not at -110 mV. When using a V(H) of -80 mV, halothane exhibited a use-dependent block, with block of I(Na) increasing from 8.6 +/- 1.4% to 30.7 +/- 3.5% at test pulse rates of 2 and 11 Hz, respectively. Use-dependent inhibition was not apparent at V(H) of -110 mV. When inactivation of I(Na) was removed by exposure to 100 microM veratridine, no significant difference was observed in the depressant effect of halothane at both V(H)s: 26.6 +/- 4.5% (V(H) = -80 mV) and 26.4 +/- 5.6% (V(H) = -110 mV). CONCLUSIONS: The present findings indicate that the depressant action of halothane on cardiac I(Na) depends on the conformational state of the channel. As more channels are in the inactivated state, the more potent is the effect of halothane. Removal of channel inactivation by veratridine abolished the dependence of the halothane effect on V(H), but depression of the current was still evident. These results indicate a complex interaction between halothane and the various conformational states of the Na+ channel.     

A noncaseating granulomatous lesion of the tonsil presenting as a malignant neoplasm

PURPOSE: Transjugular intrahepatic portosystemic shunts (TIPS) have markedly simplified the care of patients with refractory variceal bleeding. Follow-up of liver biochemical profiles, however, has not been done in a prospective fashion. PATIENTS AND METHODS: Twenty-nine patients undergoing TIPS placement for refractory variceal bleeding underwent serial laboratory tests and assessment of encephalopathy to determine the effect of TIPS. Prothrombin time and aspartate aminotransferase, alanine aminotransferase, total bilirubin, alkaline phosphatase, serum albumin, serum creatinine, and venous ammonia levels were checked prior to the procedure, at the time of discharge, and at 3 weeks, 3 months, and 6 months following the procedure. RESULTS: There was no statistically significant change in any of the obtained laboratory values at up to 6 months of follow-up. The change in aspartate aminotransferase level approached but did not reach statistical significance at the time of discharge and was thought to be secondary to hepatocellular trauma associated with the procedure. New onset of encephalopathy occurred in 18.2% of patients and was easily controlled with medical therapy. CONCLUSIONS: TIPS does not appear to have a significant effect on the liver biochemical profile with short-term follow-up. Hepatic encephalopathy does occur, however, in a significant number of patients but is easily controlled with medical therapy.     

Pulmonary infarcts can mimic pulmonary metastases from renal cancer

PURPOSE: Spontaneous regression of pulmonary metastases from renal cell carcinoma is a rare but well documented event. We present 2 recent cases that were radiographically consistent with pulmonary metastases from renal cell carcinoma but were pathologically shown to be pulmonary infarcts with no evidence of metastatic cells. Stable pulmonary infarcts can be misconstrued as metastatic disease in patients with renal cell carcinoma while resolving pulmonary infarcts may represent a subpopulation of patients with apparent spontaneous regression. Clinical implications of these findings are discussed. MATERIALS AND METHODS: Clinical and pathological data from 2 patients with large primary renal tumors, venous thrombi and lung masses were reviewed. Data from these cases, as well as pertinent urological and pathological literature, are presented. RESULTS: Although preoperative assessment was consistent with stage IV renal cell carcinoma, pathological examination of the lung masses in these patients showed no evidence of tumor cells. CONCLUSIONS: Pulmonary infarcts may mimic resolving or stable pulmonary metastasis in patients with renal cell carcinoma. Accurate clinical staging is crucial for the prognosis and treatment of renal cell carcinoma. Mistaking pulmonary infarcts for metastatic lesions can lead to inaccurate prognoses and inappropriate treatment.