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Total hydrocarbon (THC), including volatile organic compounds (VOCs), is emitted during the operations of an auto-repair painting workshop. VOCs are especially hazardous pollutants because of their impacts on ozone formation and human health. To reduce the THC generated from small auto-repair painting shops, the Korean government conducts a support program to enable them to shift from an old to a new adsorption system. Although lab-scale evaluations of the pollutant reduction efficiencies of some adsorption devices have been carried out, actual field evaluations are lacking. In this study, three auto-repair shops (one with an old and two with new air pollutant adsorption systems) in Seoul were selected to evaluate their removal efficiencies with respect to THC and VOCs during painting and drying operations. Results show that the THC removal efficiencies were − 41.3–35.4% and 17.2 − 59.2% for the old and new adsorption systems, respectively. The removal efficiencies of the top five VOC species such as butyl acetate, toluene, 1,2,3-trimethylbenzene, m,p-xylene, and ethylbenzene were positive (+) and negative (−) for the new and old adsorption systems, respectively. These results provide a theoretical basis that endorses the government support policy for the removal of air pollutants from the emissions of small businesses that are not well managed, such as auto-repair painting, printing, and dry cleaning.

The anti-cancer agent doxorubicin (DOX) has high cardiotoxicity that is linked to DOX-mediated increase in oxidative stress, mitochondrial iron overload, DNA damage, autophagy, necrosis, and apoptosis, all of which are also associated with secondary tumorigenicity. This limits the clinical application of DOX therapies. Previous studies have attributed DOX-mediated cardiotoxicity to mitochondrial iron accumulation and the production of reactive oxygen species (ROS), which seem to be independent of its anti-tumor DNA damaging effects. Chemo-sensitization of soluble guanylate cyclase (sGC) in the cyclic guanosine monophosphate (cGMP) pathway induces tumor cell death despite the cardiotoxicity associated with DOX treatment. However, sGC-cGMP signaling must be activated during heart failure to facilitate myocardial cell survival. The sGC pathway is dependent on nitric oxide and signal transduction via the nitric oxide-sGC-cGMP pathway and is attenuated in various cardiovascular diseases. Additionally, cGMP signaling is regulated by the action of certain phosphodiesterases (PDEs) that protect the heart by inhibiting PDE, an enzyme that hydrolyses cGMP to GMP activity. In this review, we discuss the studies describing the interactions between cGMP regulation and DOX-mediated cardiotoxicity and their application in improving DOX therapeutic outcomes. The results provide novel avenues for the reduction of DOX-induced secondary tumorigenicity and improve cellular autonomy during DOX-mediated cardiotoxicity.

A 0.8-V Bluetooth 5 (BT5) digitally intensive transceiver with a phase-tracking RX and a digital TX in 40-nm CMOS is presented. For the phase-tracking RX, a hybrid loop filter with a loop-delay compensation is proposed to suppress digitally controlled oscillator (DCO) sidelobe energy, enhancing interference resilience. To facilitate the DCO-based phase-tracking RX for the reception of BT5 signals, a corresponding digital baseband is implemented with a carrier frequency offset (CFO) calibration to remove the initial static CFO error during the preamble, while an automatic frequency calibration tackles the frequency drift during the payload. An all-digital phase-locked loop (ADPLL)-based digital frequency-modulation (FM) interface shared between TX and RX provides a precise deviation frequency control, ensuring the quality of signal transmission and reception. In the RX mode, the chip consumes 2.3 mW from a 0.8-V supply, achieving a figure of merit (FoM) of 180 dB with −91-/−94-dBm sensitivity at 2/1 Mb/s. In the TX mode, it consumes 6.1 mW when delivering a maximum 1.8-dBm output power, resulting in 25% TX system efficiency.

This article discusses the economic development of Belarus, which took the gradualist approach in transition. Rejecting the Washington Consensus—based reform, Belarus experienced a quick recovery during the 1990s and rapid economic growth during the early to mid-2000s. The government took various policy measures to ensure the structure of a centrally planned economy. These measures included price control, emphasis on the large state-owned enterprises, restrictions on foreign direct investment (FDI) inflows, and tariff protection. Facing limits to economic growth since the late 2000s, the government has undertaken liberalization measures including price decontrol, promotion of small and medium-sized enterprises, derestriction of FDI inflows, and trade liberalization. In the meantime, realizing the role of industrialization, it placed an emphasis on development of the manufacturing sector by lowering tariff rates imposed on capital goods. Finally, the article provides policy implications for the other developing and transition economies pursuing economic development in light of the experience of Belarus.

In this work, environmentally friendly photocatalysts with attractive catalytic properties are reported that have been prepared by introducing SnO2 quantum dots (QDs) directly onto ZnSe(N2 H4 )0.5 substrates to induce advantageous charge separation. The SnO2 /ZnSe(N2 H4 )0.5 nanocomposites could be easily synthesized through a one-pot hydrothermal process. Owing to the absence of capping ligands, the attached SnO2 QDs displayed superior photocatalytic properties, generating many exposed reactive surfaces. Moreover, the addition of a specified amount of SnO2 boosted the visible-light photocatalytic activity; however, the presence of excess SnO2 QDs in the substrate resulted in aggregation and deteriorated the performance. The spectroscopic data revealed that the SnO2 QDs act as a photocatalytic mediator and enhance the charge separation within the type II band alignment system of the SnO2 /ZnSe(N2 H4 )0.5 heterojunction photocatalysts. The separated charges in the heterojunction nanocomposites promote radical generation and react with pollutants, resulting in enhanced photocatalytic performance.

Hybrid nanoflowers consisting of graphitic carbon nitride (GCN) and copper were successfully constructed without the involvement of any biomolecule, by simply mixing them at room temperature to induce proper self-assembly to achieve a flower-like morphology. The resulting biomolecule-free GCN-copper hybrid nanoflowers (GCN-Cu NFs) exhibited an apparent peroxidase-mimicking activity, possibly owing to the synergistic effect from the coordination of GCN and copper, as well as their large surface area, which increased the number of catalytic reaction sites. The peroxidase-mimicking GCN-Cu NFs were then employed in the colorimetric determination of selected phenolic compounds hydroquinone (HQ), methylhydroquinone (MHQ), and catechol (CC). For samples without phenolic compounds, GCN-Cu NFs catalyzed the oxidation of the peroxidase substrate 3,3′,5,5′-tetramethylbenzidine (TMB) in the presence of H2O2, producing an intense blue color signal. Conversely, in the presence of phenolic compounds, the oxidation of TMB was inhibited, resulting in a significant reduction of the color signal. Using this strategy, HQ, MHQ, and CC were selectively and sensitively determined in a linear range up to 100 μM with detection limits down to 0.82, 0.27, and 0.36 μM, respectively. The practical utility of this assay system was also validated by using it to detect phenolic compounds spiked in tap water, yielding a good recovery of 97.1–108.9% and coefficient of variation below 3.0%, demonstrating the excellent reliability and reproducibility of this strategy.

Introduction Most cases of Parkinson's disease (PD) are sporadic, but genetic variations have been discovered in PD patients. PARK7/DJ-1 is a known cause of early-onset autosomal-recessive PD and is implicated in neuroprotection against oxidative stress. Although several post-translational modifications of DJ-1 have been proposed, phospho-modification of DJ-1 and its functional consequences have been less studied. Methods Putative phosphorylation sites of DJ-1 were determined by liquid chromatography-tandem mass spectrometry (LC-MS/MS analysis). Subsequently, phosphorylation site of DJ-1 was confirmed by in vitro kinase assay and cell-based pull-down assay. Impaired dimer formation of phospho-null mutant was measured using DSS crosslinking assay and immunoprecipitation assay. To evaluate physiological consequences of this event, protein stability of DJ-1 WT and DJ-1 phospho-null mutant were compared using cycloheximide chase assay and ubiquitination assay. Results Here, we showed that DJ-1 directly bound to the catalytic subunit of protein kinase A (PKAcα). We found that PKAcα is responsible for phosphorylation of DJ-1 at the T154 residue. Interestingly, dimerization of DJ-1 was not detected in a DJ-1 T154A mutant. Furthermore, stability of the DJ-1 T154A mutant was dramatically reduced compared with that of wild-type DJ-1. We found that DJ-1 T154A was prone to degradation by the ubiquitin proteasome system (UPS). Conclusion We identified a novel phosphorylation site of DJ-1. Furthermore, we determined protein kinase A that is responsible for this posttranslational modification. Finally, we demonstrated physiological consequences of this event focusing on dimerization and protein stability of DJ-1.

The catalytic oxidation of toluene with ozone at room temperature was carried out over hierarchically ordered mesoporous catalysts (CeO2 (meso), Mn2O3 (meso), ZrO2 (meso), and γ-Al2O3 (meso)) and Al2O3 with various textural properties and phases (γ-Al2O3 (meso), γ-Al2O3 (13 nm), and α-Al2O3) to examine the effects of the nature of the catalyst on the catalytic activity. The catalysts were characterized by N2-physisorption measurements, powder X-ray diffraction, temperature programmed reduction, X-ray photoelectron spectroscopy and scanning transmission electron microscopy with energy dispersive spectroscopy. Among the ordered mesoporous catalysts, γ-Al2O3 (meso) had the highest toluene removal efficiency because of its highest surface area and pore volume, which in turn was selected for further investigation. Manganese (Mn) was introduced to various Al2O3 to improve the toluene removal efficiency. Comparing the Mn-loaded catalysts supported on various Al2O3 with different crystalline phases or pore structures, Mn/γ-Al2O3 (meso), had the highest catalytic activity as well as the highest CO2/CO ratio. The higher activity was attributed to the larger surface area, weaker interaction between Mn and Al2O3, and larger portion of Mn2O3 phase. The increase in ozone concentration led to an improvement in the carbon balance but this enhancement was insufficient due to the deposition of by-products on the catalyst. After long term tests at room temperature, the reaction intermediates and carbonaceous deposits of the used catalysts were identified.

Acetaldehyde removal tests were performed to compare the catalytic activity of the Kraft lignin char (KC), KOH-treated Kraft lignin char (KKC), and activated carbon (AC) along with their impregnation with Mn in a plasma reactor. The gasification characteristics (syngas content, and H2/CO ratio) of yellow poplar were investigated using nickel catalysts supported on KC, KKC, AC, and γ-Al2O3 in a U-type quartz reactor. KKC and Mn/KKC improved significantly the surface area and contents of O and N functional groups over the raw char. In particular, Mn/KKC showed the highest acetaldehyde-removal efficiency. The catalytic activity of Ni-impregnated KC, KKC, AC, and γ-Al2O3 decreased in the order of Ni/KKC > Ni/AC > Ni/KC > Ni/γ-Al2O3 for the gas yield and Ni/γ-Al2O3 >Ni/KC > Ni/AC >Ni/KKC for the oil yield, respectively. The Ni/KKC provides a more conducive environment for gasification, resulting in larger amounts of syngas (H2 and CO) in the product gases. Moreover, Ni impregnated with char may be the most inexpensive and effective solution for achieving maximum tar reduction and syngas generation.

Studies of neuroglial interaction largely depend on cell-specific gene knockout (KO) experiments using Cre recombinase. However, genes known as glial-specific genes have recently been reported to be expressed in neuroglial stem cells, leading to the possibility that a glia-specific Cre driver results in unwanted gene deletion in neurons, which may affect sound interpretation. 2',3'-Cyclic nucleotide 3'-phosphodiesterase (CNP) is generally considered to be an oligodendrocyte (OL) marker. Accordingly, Cnp promoter-controlled Cre recombinase has been used to create OL-specific gene targeting mice. However, in this study, using Rosa26-tdTomato-reporter/Cnp-Cre mice, we found that many forebrain neurons and cerebellar Purkinje neurons belong to the lineages of Cnp-expressing neuroglial stem cells. To answer whether gene targeting by Cnp-Cre can induce neuron-autonomous defects, we conditionally deleted an essential autophagy gene, Atg7, in Cnp-Cre mice. The Cnp-Cre-mediated Atg7 KO mice showed extensive p62 inclusion in neurons, including cerebellar Purkinje neurons with extensive neurodegeneration. Furthermore, neuronal areas showing p62 inclusion in Cnp-Cre-mediated Atg7 KO mice overlapped with the neuronal lineage of Cnp-expressing neuroglial stem cells. Moreover, Cnp-Cre-mediated Atg7-KO mice did not develop critical defects in myelination. Our results demonstrate that a large population of central neurons are derived from Cnp-expressing neuroglial stem cells; thus, conditional gene targeting using the Cnp promoter, which is known to be OL-specific, can induce neuron-autonomous phenotypes.

In brain ischemia, oxidative stress induces neuronal apoptosis, which is mediated by increased activity of the voltage-gated K+ channel Kv2.1 and results in an efflux of intracellular K+. The molecular mechanisms underlying the regulation of Kv2.1 and its activity during brain ischemia are not yet fully understood. Here this study provides evidence that oxidant-induced apoptosis resulting from brain ischemia promotes rapid tyrosine phosphorylation of Kv2.1. When the tyrosine phosphorylation sites Y124, Y686, and Y810 on the Kv2.1 channel are mutated to non-phosphorylatable residues, PARP-1 cleavage levels decrease, indicating suppression of neuronal cell death. The tyrosine residue Y810 on Kv2.1 was a major phosphorylation site. In fact, cells mutated Y810 were more viable in our study than were wild-type cells, suggesting an important role for this site during ischemic neuronal injury. In an animal model, tyrosine phosphorylation of Kv2.1 increased after ischemic brain injury, with an observable sustained increase for at least 2 h after reperfusion. These results demonstrate that tyrosine phosphorylation of the Kv2.1 channel in the brain may play a critical role in regulating neuronal ischemia and is therefore a potential therapeutic target in patients with brain ischemia.

This paper presents a millimeter-scale crystal-less wireless transceiver for volume-constrained insertable pills. Operating in the 402-405 MHz medical implant communication service (MICS) band, the phase-tracking receiver-based over-the-air carrier recovery has a ±160 ppm coverage. A fully integrated adaptive antenna impedance matching solution is proposed to calibrate the antenna impedance variation inside the body. A tunable matching network (TMN) with single inductor performs impedance matching for both transmitter (TX) and receiver (RX) and TX/RX mode switching. To dynamically calibrate the antenna impedance variation over different locations and diet conditions, a loop-back power detector using self-mixing is adopted, which expands the power contour up to 4.8 VSWR. The transceiver is implemented in a 40-nm CMOS technology, occupying 2 mm2 die area. The transceiver chip and a miniature antenna are integrated in a 3.5 × 15 mm2 area prototype wireless module. It has a receiver sensitivity of-90 dBm at 200 kbps data rate and delivers up to-25 dBm EIRP in the wireless measurement with a liquid phantom.

The gastro-intestinal (GI) tract is a very important part of the human digestive system but remains largely inaccessible for unobtrusive monitoring. Ingestible electronic devices are a very interesting concept to address this need. This paper discusses the current state of ingestible electronic devices and explores the potential they hold to provide unprecedented insight by measuring several aspects of the complex bio-chemical processes that happen in the GI tract in real-time. This will require novel sensor technology capable of measuring relevant markers with adequate specificity and accuracy. In order to be able to scale this functionality down to a form factor of an easily digestible pill, ultra-low-power wireless interface electronics are needed. This poses certain challenges and innovation opportunities related to sensing, wireless communication and powering to enable the next generation of ingestible electronic devices. [2020-0164]

An on-chip DFLL (Digitally Frequency Locked Loop) based wakeup timer with a time-domain trimming featuring an embedded temperature sensor is presented. The proposed trimming exploits the deterministic temperature characteristics of two complementary resistors and results in a fine trimming step (±1ppm), allowing a small frequency error after trimming (

In this chapter, spread spectrum clock generation (SSCG)-an advanced clock generation solution for electromagnetic interference (EMI) -is presented. EMI becomes critical as the clock speed and the degree of integration are increased. Various EMI suppression techniques are introduced in this chapter. Among EMI suppression techniques, SSCG is a simple but cost-effective solution since it requires no external components and can be implemented using existing clock generators. Several SSCG design approaches are described. Similar to other clock generators, SSCG also faces implementation issues, for example, noise, non linearity, and mismatch. Finally, recent spread spectrum clocking (S SC) modulation profiles are presented and discussed because the SSC modulation profile dominates the EMI performance.

Background Doxorubicin (DOX) administration decreases cardiac soluble guanylate cyclase (sGC) activity. We hypothesized that bypassing impaired NO-sGC-cGMP pathway resulting from the activation of oxidized and heme-free soluble guanylate cyclase (sGC) could be a therapeutic target for DOX-mediated cardiomyopathy (DOX-CM). The present study investigated the therapeutic roles and mechanism of BAY60-2770, an activator of oxidized sGC, in alleviating DOX-CM. Methods H9c2 cardiomyocytes were pretreated with BAY60-2770 followed by DOX. Cell viability and intracellular reactive oxygen species (ROS) were subsequently measured. To determine the role BAY60-2770 in mitochondrial ROS generation and mitochondrial membrane potential, we examined mitoSOX RED and TMRE fluorescence under DOX exposure. As animal experiments, rats were orally administered with 5 mg/kg of BAY60-2770 at 1 h prior to every DOX treatment and then assessed by echocardiography and apoptotic marker and autophagy. Results BAY60-2770 ameliorated cell viability and DOX-induced oxidative stress in H9c2 cells, which was mediated by PKG activation. Mitochondrial ROS and TMRE fluorescence were attenuated by BAY60-2770 in DOX-treated H9c2 cells. DOX-induced caspase-3 activation decreased after pretreatment with BAY60-2770 in vivo and in vitro. Echocardiography showed that BAY60-2770 significantly improved DOX-induced myocardial dysfunction. Autophagosome was increased by BAY60-2770 in vivo. Conclusions BAY60-2770 appears to mitigate DOX-induced mitochondrial ROS, membrane potential loss, autophagy, and subsequent apoptosis, leading to protection of myocardial injury and dysfunction. These novel results highlighted the therapeutic potential of BAY60-2770 in preventing DOX-CM.

Nowadays, almost every mobile device features Bluetooth Low Energy (BLE) connectivity. Accurate RF-based ranging is of major importance to enable rapidly emerging applications such as indoor localization and navigation, asset tracking as well as secure access control. Phase-based ranging has many advantages over other methods such as Time-of-Flight or signal-strength-based approaches [1]. Phase-based ranging is based on the phase difference between the two nodes, which depends on the RF frequency. To mitigate multipath problems and deal with the 2n ambiguity in phase measurements, the phase difference is measured on multiple frequencies, i.e. Multi-Carrier Phase Difference (MCPD) [1].

Gastroscopy is a common diagnosis method for gastrointestinal (GI) diseases, but it needs to be performed in hospitals. Existing ingestible pills can collect patients' GI information over a longer period outside of a hospital, and various sensors can be incorporated to collect more information. However, ingestible pills passing through the GI system cannot make long recordings in specific places of interest. New gastroscope research focuses on the use of the biopsy channel of an insertion tube to attach the pill on a specific surface of the GI tract for some time before it detaches itself [1]. One of the most challenging parts of such “insertable” pill design is the volume constraint. The biopsy channels in gastroscopes have a diameter of ~3.5mm (at least 3x less than existing pills), and the length of the non-bendable part should be $ (10) antenna which has high sensitivity to the surrounding environment. A crystal-less transceiver is preferred because the crystal is typically the biggest off-chip component. A mm-scale radio in [3] replaces the crystal with an FBAR but requires a special manufacturing process. A mm-scale crystal-free radio in [4] presented a network-assisted timing synchronization for its Pulse-Position-Modulation(PPM)-based system. However, transceivers operating in MICS must adhere to a carrier stability better than $\pm$ 100ppm which mandates carrier synchronization for crystal-free operation, and it is especially critical for FSK/PSK transceivers that are preferred in MICS for their better channel selectivity and interference resilience. Power-oscillator topologies [5] have been widely adopted in recent mm-scale radios owing to their small size and high efficiency. However, the external coil impedance variation due to the direct contact of tissues can influence the carrier stability of the power oscillator, and the power oscillator cannot be reconfigured as an LO for FSKIPSK-based RXs.

A low-power impedance detection method using a hybrid transformer and its analysis are presented. A balun is reused for the hybrid transformer to achieve area-efficiency. The complex impedance detection enables faster optimization on a tunable matching network and its calibration technique increases the detection accuracy. The proposed impedance detection method fabricated in a 40-nm CMOS process consumes only 0.83 mW and demonstrates the accuracy of less than 18° and 0.1 on the Γ detection up to $\vert \Gamma _{{\rm{Ant}}}\vert $ of 0.5 in ISM2.4 GHz band. After single-step matching network tuning, PA power and RX noise figure are improved by up to 1.2 dB and 1.3 dB, respectively.

Objective Myelinated Schwann cells (SCs) in adult peripheral nerves dedifferentiate into immature cells in demyelinating neuropathies and Wallerian degeneration. This plastic SC change is actively involved in the myelin destruction and clearance as demyelinating SCs (DSCs). In inherited demyelinating neuropathy, pathologically differentiated and dysmyelinated SCs constitute the main nerve pathology. Methods We investigated whether this SC plastic status in human neuropathic nerves could be determined by patient sera to develop disease‐relevant serum biomarkers. Based on proteomics analysis of the secreted exosomes from immature SCs, we traced p75 neurotrophin receptor (p75) and neural cell adhesion molecule 1 (NCAM) in the sera of patients with peripheral neuropathy. Results Enzyme‐linked immunosorbent assay (ELISA) revealed that p75 and NCAM were subtype‐specifically expressed in the sera of patients with peripheral neuropathy. In conjunction with these ELISA data, pathological analyses of animal models and human specimens suggested that the presence of DSCs in inflammatory neuropathy and of supernumerary nonmyelinating or dysmyelinating SCs in inherited neuropathy could potentially be distinguished by comparing the expression profiles of p75 and NCAM. Interpretation This study indicates that the identification of disease‐specific pathological SC stages might be a valuable tool for differential diagnosis of peripheral neuropathies.

Photocatalytic hydrogen (H2) production on zinc sulfide (ZnS) still remains unsatisfactory because of the fast charge carrier recombination through direct-bandgap and photocorrosion by oxidative holes at the valence band. Here we report on a strongly coupled heterojunction photocatalyst (ZnS/PDA) comprising by a ZnS nanorod and ultrathin polydopamine (PDA). The ZnS/PDA exhibits H2 production rate of 2162.5 μmol h−1 g−1, and 78.7 % of this initial photoactivity is sustained after consecutive running for 24 h. A double staggered heterostructure by interfacial zinc oxysulfide and 1 nm-thick PDA layer gives rise to the effective separation, transport, and tunneling of charge carriers for robust H2 production without the trade-off between photocatalytic stability and activity. We anticipate that the present ZnS/PDA can be exploitable in other catalytic applications, such as disinfection of bacteria and air purification. Furthermore, easy modification of optoelectronic properties by PDA will be applicable to a wide range of materials.

Background A number of reports have described the protective effects of ginsenoside Rg1 (Rg1) in Alzheimer's disease (AD). However, the protective mechanisms of Rg1 in AD remain elusive. Methods To investigate the potential mechanisms of Rg1 in β-amyloid peptide-treated SH-SY5Y cells, a comparative proteomic analysis was performed using stable isotope labeling with amino acids in cell culture combined with nano-LC-MS/MS. Results We identified a total of 1,149 proteins in three independent experiments. Forty-nine proteins were significantly altered by Rg1 after exposure of the cells to β-amyloid peptides. The protein interaction network analysis showed that these altered proteins were clustered in ribosomal proteins, mitochondria, the actin cytoskeleton, and splicing proteins. Among these proteins, mitochondrial proteins containing HSD17B10, AARS2, TOMM40, VDAC1, COX5A, and NDUFA4 were associated with mitochondrial dysfunction in the pathogenesis of AD. Conclusion Our results suggest that mitochondrial proteins may be related to the protective mechanisms of Rg1 in AD.

We developed TiO2 particles conjugated with an Escherichia coli surface-specific ssDNA aptamer cocktail (composed of three different aptamers isolated from E. coli) for targeted and enhanced disinfection of E. coli. We examined the target-specific and enhanced inactivation of this composite (TiO2-Apc), which were compared to those of TiO2 conjugated with a single aptamer (one of the three different aptamers, TiO2-Aps) and non-modified TiO2. We found that TiO2-Apc enhanced the inactivation of targeted E. coli under UV irradiation compared to both the non-modified TiO2 and TiO2-Aps. A higher number of TiO2-Apc than TiO2-Aps particles was observed on the surface of E. coli. The amount of TiO2-Apc required to inactivate ∼99.9% of E. coli (106 CFU/ml) was 10 times lower than that of non-modified TiO2. The close proximity of functionalized particles with E. coli resulting from the interaction between the target surface and the aptamer induced the efficient and fast transfer of reactive oxygen species to the cells. In a mixed culture of different bacteria (E. coli and Staphylococcus epidermidis), TiO2-Apc enhanced the inactivation of only E. coli. Taken together, these results support the use of aptamer cocktail-conjugated TiO2 for improvement of the target-specific inactivation of bacteria.

There are many studies portraying iron (Fe) and nitrogen (N)-functionalzed carbon as an electrocatalyst along with possible elucidation of catalytically active sites. Despite continuous controversial debate on the active sites/species, the presence of N is believed to be undeniably needed for the efficient catalysis, whereas the necessity and role of Fe are still debated. To clearly understand the role of Fe in Fe and N-functionalized electrocatalyst, N-doped hollow mesoporous shell carbon (N-HMSC) is prepared as a uniform model electrocatalyst by a simple template nanocasting using Fe phthalocyanine (FePc) as a single precursor for carbon, N, and Fe. It is found that the presence of Fe in N-HMSC leads to the efficient graphitization of N-HMSC structure, which can be beneficial for electrocatalytic oxygen evolution reaction (OER). Interestingly, it is observed that Fe is a must for the preparation of high efficient catalyst, but may not be necessary for OER.