A New Method of Bio-Catalytic Surface Modification for Microbial Desalination Cell

A microbial desalination cell (MDC) built on a modified surface has been studied for seawater desalination. The goal of this study is to provide and develop a seawater desalination system that does not require energy support by applying a modification of the anode as an electron acceptor. The different potential charges that occur between anode and cathode can serve as the driving force for electrodialysis of seawater, resulting in its desalination. Yeast has been applied as a biocatalyst and neutral red has been chosen as a redox mediator to facilitate the electron transport originating from the bioactivity of cells. Several types of surface modification have been conducted, i.e., biocatalyst-mediator immobilisation and electropolymerisation of neutral red at the anode surface. The optimisation of each device has been characterised by cyclic voltammetry and chronoamperometry. It has also been observed in a microbial fuel cell (MFC), prior to being functioned in the MDC. The concentrations of salt ion migration have been determined by ion exchange chromatography. This study found that the best configuration of a modified surface was obtained from carbon felt coated by polyneutral red film (CF/PNR); this generated the maximum value of all tested parameters: 42.2% of current efficiency; 27.11% of bio-devices efficiency; 92.5 mA m-2 of current density; and 61% of NaCl transport. Moreover, the modified surface could be a promising method for improving anode performance.

A New Method of Bio-Catalytic Surface Modification For Microbial Desalination Cell

Microbial desalination cell (MDC) built on surface modification has been studied for seawater desalination. Herein, the bio-catalytic surface modification for maintenance the long-term MDC performance during desalination process has been developed. The goal of this study is to provide and develop a seawater desalination system without requiring energy support by applying a modification of anode as an electron acceptor, and the different potential charges that occur between anode and cathode can play as driving force for electrodialysis of seawater desalination. Yeast has been applied as biocatalyst, meanwhile neutral red has been chosen as redox mediator to facilitate the electron transport from bioactivity of cells. Several types of surface modification have been conducted, i.e. biocatalyst-mediator immobilization and electropolymerization of NR at the surface of the anode. The optimization of each device has been characterized by cyclic voltammetry, chronoamperometry, and observed in Microbial fuel cell (MFC) prior functioned in MDC. The concentrations of salt ion migration have been determined by Ion Exchange Chromatography. MFC results reported that the best configuration of surface modification was obtained from CF/PNR then applied in MDC. CF/PNR delivered the highly significant performance by having the maximum value of all tested parameters, i.e 42.2% of current efficiency; 27.11% of bio-devices efficiency; 92.5 mA m-2 of current density and also 61% of NaCl transport. The profiles of surface devices have been detected by Scanning electron microscope (SEM) and Energy Dispersive X-ray spectroscopy (EDX). A several spherical shapes around 4 nm within alginate layer have been detected from SEM images and it was confirmed as yeast, meanwhile 5.04% of N has been found from EDX spectrum and was indicated from PNR. The results show that surface modification could be a promising method for bioelectricity generation which simultaneously produces electricity and seawater desalination and provides a green chemistry technology.

A new method of bio-catalytic surface modification for microbial desalination cell

Microbial desalination cell (MDC) built on surface modification has been studied for seawater desalination. Herein, the bio-catalytic surface modification for maintenance the long-term MDC performance during desalination process has been developed. The goal of this study is to provide and develop a seawater desalination system without requiring energy support by applying a modification of anode as an electron acceptor, and the different potential charges that occur between anode and cathode can play as driving force for electrodialysis of seawater desalination. Yeast has been applied as biocatalyst, meanwhile neutral red has been chosen as redox mediator to facilitate the electron transport from bioactivity of cells. Several types of surface modification have been conducted, i.e. biocatalyst-mediator immobilization and electropolymerization of NR at the surface of the anode. The optimization of each device has been characterized by cyclic voltammetry, chronoamperometry, and observed in Microbial fuel cell (MFC) prior functioned in MDC. The concentrations of salt ion migration have been determined by Ion Exchange Chromatography. MFC results reported that the best configuration of surface modification was obtained from CF/PNR then applied in MDC. CF/PNR delivered the highly significant performance by having the maximum value of all tested parameters, i.e 42.2% of current efficiency; 27.11% of bio-devices efficiency; 92.5 mA m-2 of current density and also 61% of NaCl transport. The profiles of surface devices have been detected by Scanning electron microscope (SEM) and Energy Dispersive X-ray spectroscopy (EDX). A several spherical shapes around 4 nm within alginate layer have been detected from SEM images and it was confirmed as yeast, meanwhile 5.04% of N has been found from EDX spectrum and was indicated from PNR. The results show that surface modification could be a promising method for bioelectricity generation which simultaneously produces electricity and seawater desalination and provides a green chemistry technology.

A mathematical model of the rat kidney. II. Antidiuresis

Kidney water conservation requires a hypertonic medullary interstitium, NaCl in the outer medulla and NaCl and urea in the inner medulla, plus a vascular configuration that protects against washout. In this work, a multisolute model of the rat kidney is revisited to examine its capacity to simulate antidiuresis. The first step was to streamline model computation by parallelizing its Jacobian calculation, thus allowing finer medullary spatial resolution and more extensive examination of model parameters. It is found that outer medullary NaCl is modestly increased when transporter density in ascending Henle limbs from juxtamedullary nephrons is scaled to match the greater juxtamedullary solute flow. However, higher NaCl transport produces greater CO2 generation and, by virtue of countercurrent vascular flows, establishment of high medullary Pco2. This CO2 gradient can be mitigated by assuming that a fraction of medullary transport is powered anaerobically. Reducing vascular flows or increasing vessel permeabilities does little to further increase outer medullary solute gradients. In contrast to medullary models of others, vessels in this model have solute reflection coefficients close to zero; increasing these coefficients provides little enhancement of solute profiles but does generate high interstitial pressures, which distort tubule architecture. Increasing medullary urea delivery via entering vasa recta increases inner medullary urea, although not nearly to levels found in rats. In summary, 1) medullary Na+ and urea gradients are not captured by the model and 2) the countercurrent architecture that provides antidiuresis also produces exaggerated Pco2 profiles and is an unappreciated constraint on models of medullary function.

Characterization of renal NaCl and oxalate transport in Slc26a6−/− mice

The apical membrane Cl−/oxalate exchanger SLC26A6 has been demonstrated to play a role in proximal tubule NaCl transport based on studies in microperfused tubules. The present study is directed at characterizing the role of SLC26A6 in NaCl homeostasis in vivo under physiological conditions. Free-flow micropuncture studies revealed that volume and Cl− absorption were similar in surface proximal tubules of wild-type and Slc26a6−/− mice. Moreover, the increments in urine flow rate and sodium excretion following thiazide and furosemide infusion were identical in wild-type and Slc26a6−/− mice, indicating no difference in NaCl delivery out of the proximal tubule. The absence of an effect of deletion of SLC26A6 on NaCl homeostasis was further supported by the absence of lower blood pressure in Slc26a6−/− compared with wild-type mice on normal or low-salt diets. Moreover, raising plasma and urine oxalate by feeding mice a diet enriched in soluble oxalate did not affect mean blood pressure. In contrast to the lack of effect of SLC26A6 deletion on NaCl homeostasis, fractional excretion of oxalate was reduced from 1.6 in wild-type mice to 0.7 in Slc26a6−/− mice. We conclude that, although SLC26A6 is dispensable for renal NaCl homeostasis, it is required for net renal secretion of oxalate.

Role of connecting tubule glomerular feedback in obesity related renal damage

Zucker obese rats (ZOR) have higher glomerular capillary pressure (PGC) that can cause renal damage. PGC is controlled by afferent (Af-Art) and efferent arteriole (Ef-Art) resistance. Af-Art resistance is regulated by factors that regulate other arterioles, such as myogenic response. In addition, it is also regulated by 2 intrinsic feedback mechanisms: 1) tubuloglomerular feedback (TGF) that causes Af-Art constriction in response to increased NaCl in the macula densa and 2) connecting tubule glomerular feedback (CTGF) that causes Af-Art dilatation in response to an increase in NaCl transport in the connecting tubule via the epithelial sodium channel. Since CTGF is an Af-Art dilatory mechanism, we hypothesized that increased CTGF contributes to TGF attenuation, which in turn increases PGC in ZOR. We performed a renal micropuncture experiment and measured stop-flow pressure (PSF), which is an indirect measurement of PGC in ZOR. Maximal TGF response at 40 nl/min was attenuated in ZOR (4.47 ± 0.60 mmHg) in comparison to the Zucker lean rats (ZLR; 8.54 ± 0.73 mmHg, P < 0.05), and CTGF was elevated in ZOR (5.34 ± 0.87 mmHg) compared with ZLR (1.12 ± 1.28 mmHg, P < 0.05). CTGF inhibition with epithelial sodium channel blocker normalized the maximum PSF change in ZOR indicating that CTGF plays a significant role in TGF attenuation (ZOR, 10.67 ± 1.07 mmHg vs. ZLR, 9.5 ± 1.53 mmHg). We conclude that enhanced CTGF contributes to TGF attenuation in ZOR and potentially contribute to progressive renal damage.

Connecting tubule glomerular feedback mediates tubuloglomerular feedback resetting after unilateral nephrectomy

Unilaterally nephrectomized rats (UNx) have higher glomerular capillary pressure (PGC) that can cause significant glomerular injury in the remnant kidney. PGC is controlled by the ratio of afferent (Af-Art) and efferent arteriole resistance. Af-Art resistance in turn is regulated by two intrinsic feedback mechanisms: 1) tubuloglomerular feedback (TGF) that causes Af-Art constriction in response to increased NaCl in the macula densa; and 2) connecting tubule glomerular feedback (CTGF) that causes Af-Art dilatation in response to an increase in NaCl transport in the connecting tubule via the epithelial sodium channel (ENaC). Resetting of TGF post-UNx can allow systemic pressure to be transmitted to the glomerulus and cause renal damage, but the mechanism behind this resetting is unclear. Since CTGF is an Af-Art dilatory mechanism, we hypothesized that CTGF is increased after UNx and contributes to TGF resetting. To test this hypothesis, we performed UNx in Sprague-Dawley (8) rats. Twenty-four hours after surgery, we performed micropuncture of individual nephrons and measured stop-flow pressure (PSF). PSF is an indirect measurement of PGC. Maximal TGF response at 40 nl/min was 8.9 ± 1.24 mmHg in sham-UNx rats and 1.39 ± 1.02 mmHg in UNx rats, indicating TGF resetting after UNx. When CTGF was inhibited with the ENaC blocker benzamil (1 μM/l), the TGF response was 12.29 ± 2.01 mmHg in UNx rats and 13.03 ± 1.25 mmHg in sham-UNx rats, indicating restoration of the TGF responses in UNx. We conclude that enhanced CTGF contributes to TGF resetting after UNx.