Electrogenic Na/HCO3 Cotransporter (NBCe1) Variants Expressed in Xenopus Oocytes: Functional Comparison and Roles of the Amino and Carboxy Termini

Using pH- and voltage-sensitive microelectrodes, as well as the two-electrode voltage-clamp and macropatch techniques, we compared the functional properties of the three NBCe1 variants (NBCe1-A, -B, and -C) with different amino and/or carboxy termini expressed in Xenopus laevis oocytes. Oocytes expressing rat brain NBCe1-B and exposed to a CO2/HCO3− solution displayed all the hallmarks of an electrogenic Na+/HCO3− cotransporter: (a) a DIDS-sensitive pHi recovery following the initial CO2-induced acidification, (b) an instantaneous hyperpolarization, and (c) an instantaneous Na+-dependent outward current under voltage-clamp conditions (−60 mV). All three variants had similar external HCO3− dependencies (apparent KM of 4–6 mM) and external Na+ dependencies (apparent KM of 21–36 mM), as well as similar voltage dependencies. However, voltage-clamped oocytes (−60 mV) expressing NBCe1-A exhibited peak HCO3−-stimulated NBC currents that were 4.3-fold larger than the currents seen in oocytes expressing the most dissimilar C variant. Larger NBCe1-A currents were also observed in current–voltage relationships. Plasma membrane expression levels as assessed by single oocyte chemiluminescence with hemagglutinin-tagged NBCs were similar for the three variants. In whole-cell experiments (Vm = −60 mV), removing the unique amino terminus of NBCe1-A reduced the mean HCO3−-induced NBC current 55%, whereas removing the different amino terminus of NBCe1-C increased the mean NBC current 2.7-fold. A similar pattern was observed in macropatch experiments. Thus, the unique amino terminus of NBCe1-A stimulates transporter activity, whereas the different amino terminus of the B and C variants inhibits activity. One or more cytosolic factors may also contribute to NBCe1 activity based on discrepancies between macropatch and whole-cell currents. While the amino termini influence transporter function, the carboxy termini influence plasma membrane expression. Removing the entire cytosolic carboxy terminus of NBCe1-C, or the different carboxy terminus of the A/B variants, causes a loss of NBC activity due to low expression at the plasma membrane

A Large Open Dataset from the Parler Social Network

Parler is as an ``alternative'' social network promoting itself as a service that allows to ``speak freely and express yourself openly, without fear of being deplatformed for your views.'' Because of this promise, the platform become popular among users who were suspended on mainstream social networks for violating their terms of service, as well as those fearing censorship. In particular, the service was endorsed by several conservative public figures, encouraging people to migrate from traditional social networks. After the storming of the US Capitol on January 6, 2021, Parler has been progressively deplatformed, as its app was removed from Apple/Google Play stores and the website taken down by the hosting provider. This paper presents a dataset of 183M Parler posts made by 4M users between August 2018 and January 2021, as well as metadata from 13.25M user profiles. We also present a basic characterization of the dataset, which shows that the platform has witnessed large influxes of new users after being endorsed by popular figures, as well as a reaction to the 2020 US Presidential Election. We also show that discussion on the platform is dominated by conservative topics, President Trump, as well as conspiracy theories like QAnon

Microwave Electronics

Contains research objectives and reports on five research projects

2x2 MIMO-OFDM Gigabit fiber-wireless access system based on polarization division multiplexed WDM-PON

We propose a spectral efficient radio over wavelength division multiplexed passive optical network (WDM-PON) system by combining optical polarization division multiplexing (PDM) and wireless multiple input multiple output (MIMO) spatial multiplexing techniques. In our experiment, a training-based zero forcing (ZF) channel estimation algorithm is designed to compensate the polarization rotation and wireless multipath fading. A 797 Mb/s net data rate QPSK-OFDM signal with error free ( We propose a spectral efficient radio over wavelength division multiplexed passive optical network (WDM-PON) system by combining optical polarization division multiplexing (PDM) and wireless multiple input multiple output (MIMO) spatial multiplexing techniques. In our experiment, a training-based zero forcing (ZF) channel estimation algorithm is designed to compensate the polarization rotation and wireless multipath fading. A 797 Mb/s net data rate QPSK-OFDM signal with error free (<1 × 10−5) performance and a 1.59 Gb/s net data rate 16QAM-OFDM signal with BER performance of 1.2 × 10−2 are achieved after transmission of 22.8 km single mode fiber followed by 3 m and 1 m air distances, respectively

MIMO-OFDM WDM PON with DM-VCSEL for femtocells application

Globalization, rapid technological changes, and growing competition not only facilitate but also make the supply chain more complex and fragile. Any disruption can disturb many organizations and even the whole system. There are many theories and frameworks that present a solution but no study is available that theoretically development framework for supply chain risk management. The focus of this study is to develop a novel framework for identifying the potential risks and assessment of their effects on supply chain performance. Additionally, evaluate the role of supply chain interaction in risk mitigation and performance improvement in Malaysian manufacturing. This is a conceptual paper, systematic as well as content analysis have been done for the literature review. For future study, there is a need to empirically verification of this theoretical framework. The proposed methodology to achieve this framework is; a questionnaire will be developed from a pool and will be validated by exploratory view for risk identification. This questionnaire will be distributed among Malaysian manufacturing and data will be analyzed through Structural Equation Modelling (SEM) for risk assessment and mitigation. The theoretical contribution of this study is support of the theory of swift, even flow as underpinning theory and information processing theory as supportive theory

Sustained Na⁺/H⁺ exchanger activation promotes gliotransmitter release from reactive hippocampal astrocytes following oxygen-glucose deprivation

Hypoxia ischemia (HI)-related brain injury is the major cause of long-term morbidity in neonates. One characteristic hallmark of neonatal HI is the development of reactive astrogliosis in the hippocampus. However, the impact of reactive astrogliosis in hippocampal damage after neonatal HI is not fully understood. In the current study, we investigated the role of Na +/H+ exchanger isoform 1 (NHE1) protein in mouse reactive hippocampal astrocyte function in an in vitro ischemia model (oxygen/glucose deprivation and reoxygenation, OGD/REOX). 2 h OGD significantly increased NHE1 protein expression and NHE1-mediated H+ efflux in hippocampal astrocytes. NHE1 activity remained stimulated during 1-5 h REOX and returned to the basal level at 24 h REOX. NHE1 activation in hippocampal astrocytes resulted in intracellular Na+ and Ca2+ overload. The latter was mediated by reversal of Na+/Ca2+ exchange. Hippocampal astrocytes also exhibited a robust release of gliotransmitters (glutamate and pro-inflammatory cytokines IL-6 and TNFα) during 1-24 h REOX. Interestingly, inhibition of NHE1 activity with its potent inhibitor HOE 642 not only reduced Na+ overload but also gliotransmitter release from hippocampal astrocytes. The noncompetitive excitatory amino acid transporter inhibitor TBOA showed a similar effect on blocking the glutamate release. Taken together, we concluded that NHE1 plays an essential role in maintaining H + homeostasis in hippocampal astrocytes. Over-stimulation of NHE1 activity following in vitro ischemia disrupts Na+ and Ca2+ homeostasis, which reduces Na+-dependent glutamate uptake and promotes release of glutamate and cytokines from reactive astrocytes. Therefore, blocking sustained NHE1 activation in reactive astrocytes may provide neuroprotection following HI. © 2014 Cengiz et al