Search

When infected by Helicobacter pylori, it often causes gastritis, gastric ulcer, or gastric cancer. Antibiotics are used to treat H. pylori infection, as they inhibit or kill H. pylori often ex-tending to reduce the incidences of gastric adenoma and cancer. However, H. pylori has developed drug resistance to many clinically used antibiotics over the years, thereby providing no warranty of successful treatment whenever H. pylori infection befalls. We report here that fucoidan from Sargassumhemiphyllum can effectively reduce infection of H. pylori without development of drug resistance. Fucoidan demonstrated a strong anti-inflammation activity in RAW264.7 cell model. Using AGS cell model, fucoidan decreased H. pylori adhesion to host cells and thus reduced its infection rate, especially in post-treatment where the infection rate was reduced to 40%. Mechanistically, fucoidan intervenes the proper functions of adhesion molecules BabA and AlpA of H. pylori. Moreover, fucoidan is able to significantly lower the total count of H. pylori and the levels of IL-6 and TNF-α in vivo. Added together, these convergent results suggest that fucoidan is an effective agent in a position to protect stomach from H. pylori infection by reducing its total count and induced inflammation.

This study designs and implements a wheeled bipedal robot (WBR) that combines the mobility of wheeled robots and the dexterity of legged robots. The designed WBR has extra knee joints to maintain body balance when encountering uneven terrain. Because of the robot’s highly nonlinear, dynamic, unstable, and under-actuated nature, an intelligent motion and balance controller (IMBC) based on a fuzzy logic approach is proposed to maintain the balance of the WBR while it is standing and moving on the ground. It should be emphasized that the proposed IMBC system does not require prior knowledge of system dynamics and the controller parameters are tuned using the qualitative aspects of human knowledge. Furthermore, a 32-bit microcontroller that has memory, programmable I/O peripherals, and a processor core is used to implement the IMBC method. Finally, moving and rotating, height-changing, posture-keeping, and “one leg on slope” movement scenarios are tested to demonstrate the feasibility of the proposed IMBC system. The experimental results show that, by using the proposed IMBC system, the WBR can not only balance and move well both on flat ground and in complex terrain but also extend each leg independently to maintain body balance.

Objective To explore the effects of interleukin-6 (IL-6) gene knockout on the cognitive function and pathological changes in 5×FAD transgenic mice of Alzheimer's disease.Methods IL-6

Understanding mechanisms of cooperation between oncogenes is critical for the development of novel therapies and rational combinations. Acute myeloid leukemia (AML) cells with KMT2A-fusions and KMT2A partial tandem duplications (KMT2APTD) are known to depend on the histone methyltransferase DOT1L, which methylates histone 3 lysine 79 (H3K79). About 30% of KMT2APTD AMLs carry mutations in IDH1/2 (mIDH1/2). Previous studies showed that 2-hydroxyglutarate produced by mIDH1/2 increases H3K79 methylation, and mIDH1/2 patient samples are sensitive to DOT1L inhibition. Together, these findings suggested that stabilization or increases in H3K79 methylation associated with IDH mutations support the proliferation of leukemias dependent on this mark. However, we found that mIDH1/2 and KMT2A alterations failed to cooperate in an experimental model. Instead, mIDH1/2 and 2-hydroxyglutarate exert toxic effects, specifically on KMT2A-rearranged AML cells (fusions/partial tandem duplications). Mechanistically, we uncover an epigenetic barrier to efficient cooperation; mIDH1/2 expression is associated with high global histone 3 lysine 79 dimethylation (H3K79me2) levels, whereas global H3K79me2 is obligate low in KMT2A-rearranged AML. Increasing H3K79me2 levels, specifically in KMT2A-rearrangement leukemias, resulted in transcriptional downregulation of KMT2A target genes and impaired leukemia cell growth. Our study details a complex genetic and epigenetic interaction of 2 classes of oncogenes, IDH1/2 mutations and KMT2A rearrangements, that is unexpected based on the high percentage of IDH mutations in KMT2APTD AML. KMT2A rearrangements are associated with a trend toward lower response rates to mIDH1/2 inhibitors. The substantial adaptation that has to occur for 2 initially counteracting mutations to be tolerated within the same leukemic cell may provide at least a partial explanation for this observation.

Leukemias bearing fusions of the AF10/MLLT10 gene are associated with poor prognosis, and therapies targeting these fusion proteins (FPs) are lacking. To understand mechanisms underlying AF10 fusion-mediated leukemogenesis, we generated inducible mouse models of acute myeloid leukemia (AML) driven by the most common AF10 FPs, PICALM/CALM-AF10 and KMT2A/MLL-AF10, and performed comprehensive characterization of the disease using transcriptomic, epigenomic, proteomic, and functional genomic approaches. Our studies provide a detailed map of gene networks and protein interactors associated with key AF10 fusions involved in leukemia. Specifically, we report that AF10 fusions activate a cascade of JAK/STAT-mediated inflammatory signaling through direct recruitment of JAK1 kinase. Inhibition of the JAK/STAT signaling by genetic Jak1 deletion or through pharmacological JAK/STAT inhibition elicited potent antioncogenic effects in mouse and human models of AF10 fusion AML. Collectively, our study identifies JAK1 as a tractable therapeutic target in AF10-rearranged leukemias.

Atopic dermatitis (AD) is a long-term allergic skin disorder that occurs most frequently in children. Currently, the common treatment of AD is corticosteroids; however, the drugs cause serious side effects. Therefore, there are many patients who seek complementary and alternative treatments such as healthy food. We report that fucoidan from Cladosiphon okamuranus (COP) exhibit exceptional immuno-modulatory effects significantly improving atopic dermatitis (AD) at both in vitro and in vivo levels: First, we performed the P815 cell degranulation assay, of which the results revealed that COP possesses anti-degranulation activity suggesting COP is very conducive to relieving allergic reactions of AD. Next, we performed the animal model examination, of which AD was significantly improved, suggesting COP can focally and globally modulate the immune systems of animals. The systemic improvements were manifested clearly by decreased epidermal hyperplasia, reduced infiltration of eosinophils, and decreased expression of AD-associated cytokines. Notably, COP reduced epidermal hyperplasia by downregulating the expression of IL-22. COP displayed therapeutic effects, which is comparable to corticosteroids but lack corticosteroid side effects, such as weight loss in our animal study. COP is multitudinous immunomodulatory abilities to serve as a healthy food supplement at the current stage, not least beneficial to atopic dermatitis.

The globo-series glycosphingolipids (GSLs) SSEA3, SSEA4, and Globo-H specifically expressed on cancer cells are found to correlate with tumor progression and metastasis, but the functional roles of these GSLs and the key enzyme β1,3-galactosyltransferase V (β3GalT5) that converts Gb4 to SSEA3 remain largely unclear. Here we show that the expression of β3GalT5 significantly correlates with tumor progression and poor survival in patients, and the globo-series GSLs in breast cancer cells form a complex in membrane lipid raft with caveolin-1 (CAV1) and focal adhesion kinase (FAK) which then interact with AKT and receptor-interacting protein kinase (RIP), respectively. Knockdown of β3GalT5 disrupts the complex and induces apoptosis through dissociation of RIP from the complex to interact with the Fas death domain (FADD) and trigger the Fas-dependent pathway. This finding provides a link between SSEA3/SSEA4/Globo-H and the FAK/CAV1/AKT/RIP complex in tumor progression and apoptosis and suggests a direction for the treatment of breast cancer, as demonstrated by the combined use of antibodies against Globo-H and SSEA4.

This study Development a high-speed data acquisition (DAQ) device by using AD9226 analog-to-digital converters, a field programmable gate array, and an ARM Cortex-A8 microprocessor for a self-designed synchronous 6-channel high-speed DAQ card that was able to transmit data to a computer through its network interface. Its cost was approximately 10% that of a commercial model, the National Instruments PXI-5105, and thus overcame the prohibitively high cost of commercial DAQ cards. A high-frequency current transformer (HFCT) was used to measure three types of typical partial discharge (PD) in self-made models to compare the performance of the self-designed DAQ card and that of the National Instruments PXI-5105. The HFCT signals were converted into three-dimensional PD patterns, and mean discharge was chosen as the feature to be extracted for the application of extension theory in the recognition of discharge models. The results revealed that the self-designed DAQ card was comparable to the commercial model in the recognition of high-frequency PD signals. Given the high price of commercial high-speed DAQ devices, the self-designed DAQ card was deemed to have considerable advantages in cost and expandability.

The use of conventional fabrication methods rapidly developed the performance and notable enhancements of optoelectronic devices. However, it proved challenging to develop and demonstrate stable optoelectronic devices with biodegradability and biocompatibility properties towards sustainable development and extensive applications. This study incorporates a water-soluble Cr-phycoerythrin (Cr-PE) biomaterial to observe its optical and electronic properties effects on the pristine indium gallium zinc oxide (IGZO)-based photodetector. The fabricated photodetector demonstrates an extended absorption detection region, enhanced optoelectronic performance, and switchable function properties. The resulting photocurrent and responsivity of the IGZO/Cr-PE structure have increased by 5.7 and 7.1 times as compared to the pristine IGZO photodetector. It was also observed that the photodetector could operate in UV and UV–visible with enhanced optical properties by effectively adding the water-soluble Cr-PE. Also, the sensing region of IGZO photodetector becomes changeable. It exhibits switchable dual detection by alternatively dripping and removing the Cr-PE on the IGZO layer. Different measurement parameters such as detectivity, repeatability, and sensitivity are highlighted to effectively prove the advantage of including Cr-PE on the photodetector structure. This study contributes to understanding the potential functions in improving optoelectronic devices through an environmental-friendly method.

Leukemias bearing fusions of the AF10/MLLT10 gene are associated with poor prognosis, and therapies targeting these fusion proteins are lacking. To understand mechanisms underlying AF10 fusion-mediated leukemogenesis, we generated inducible mouse models of AML driven by the most common AF10 fusion proteins, PICALM/CALM-AF10 and KMT2A/MLL-AF10, and performed comprehensive characterization of the disease using transcriptomic, epigenomic, proteomic, and functional genomic approaches. Our studies provide a comprehensive map of gene networks and protein interactors associated with key AF10 fusions involved in leukemia. Specifically, we report that AF10 fusions activate a cascade of JAK/STAT-mediated inflammatory signaling through direct recruitment of JAK1 kinase. Inhibition of the JAK/STAT signaling by genetic Jak1 deletion or through pharmacological JAK/STAT inhibition elicited potent anti-oncogenic effects in mouse and human models of AF10 fusion AML. Collectively, our study identifies JAK1 as a tractable therapeutic target in AF10-rearranged leukemias.STATEMENT OF SIGNIFICANCEGene fusions of AF10/MLLT10 are recurrent in acute myeloid and lymphoid leukemia and are associated with extremely poor survival outcomes. We show that the JAK1 kinase is required for activation of the AF10 fusion oncotranscriptome and for leukemogenesis. Since a number of JAK/STAT pathways inhibitors are in clinical development or approved for use, our studies may help develop a therapeutic strategy for AF10-rearranged leukemias.

This study was aimed to develop a simple, fast, and reliable technique to detect fluoroquinolones (FQs)-conjugated bovine serum albumin (BSA). Four tested FQs, enrofloxacin, ofloxacin, danofloxacin, and orbifloxacin, were conjugated with BSA by following the N-hydroxysuccinimide ester method. The technique was designed according to the different absorption characteristics of the FQs and BSA; FQs can be detected by both UV and fluorescence detectors, but BSA can only be detected by UV. The results demonstrated that the developed method was efficient in detecting FQs-BSA conjugates. In addition, the method not only trace the FQs and BSA conjugation responses but also can be used to estimate the level of FQs-BSA conjugation. Therefore, this technique is a valuable tool for the detection drug-carrier-conjugated antigens, especially for FQs-BSA-conjugates during the production of anti-FQs monoclonal antibodies.

We analyzed the residual of oxolinic acid in the serum and muscle of the Chinese mitten crab by high-performance liquid chromatography (HPLC) coupled with a fluorescence detector. A standard solution of oxolinic acid was prepared by dilution with 0.05 M phosphate buffered saline (PBS) (pH 7.4). Serum and muscle samples were completely homogenized prior to addition of oxolinic acid. Samples were then transferred into an ultrasonic water bath and centrifuged. The supernatants of serum and water layer of hexane defatted muscle were passed through C-18 solid phase extraction columns. Finally, oxolinic acid in the column was eluted with methanol/NH4OH (75:25 v/v), and then was evaporated to dry by nitrogen gas. Extracted oxolinic acid was determined by HPLC with a fluorescence detector (excitation/emission=335 nm/378 nm) and a Cosmosil 5C18-MS reverse phase column (5 μm, 4.6×150 mm i.d.). A mixture of acetonitrile and 0.02 M PBS pH 3.0 (25:75) was used as the mobile phase at a flow rate of 1.0 mL/min. A peak with retention time around 8 min was observed. With the addition of 100 μg L^(-1) oxolinic acid treatments, the mean recoveries from serum and muscle were 92% and 82%, respectively. The detection limit was 1 ppb and standard curves spiked at different levels showed a good linear correlation coefficient (R(superscript 2)＞0.999 for oxolinic acid). Because residual oxolinic acid could not be detected in all tested crabs initially, five crabs were fed with oxolinic acid for 7 days by oral administration on purpose and the residual oxolinic acid in both sera and muscle were measured, respectively. The results showed that the residual oxoilinic acid in both sera and muscle could be quantified by this method. Therefore, our developed technique may be employed as a practical method for detection of residual oxolinic acid residue in Chinese mitten crabs or other aquaculture products.

Atopic dermatitis (AD) is a T helper (Th) 2 cell-mediated allergic disease, which features increased number of immunocytes and level of Th2-associated cytokines. Fucoidan is well known a naturally occurring agent effectively ameliorating many AD symptoms. Though these alleviative effects are exhilarating, the mechanisms behind, however, are still rather limited. In this study, we report that fucoidan derived from Cladosiphon okamuranus (FT) inhibits nitric oxide (NO) production by exerting its anti-inflammatory ability. Topical application on animals show that FT promotes skin repair, reduces immunocyte proliferation, and decreases serum IgE level. In histological analysis, FT favorably reduces epidermal hyperplasia and eosinophilic infiltration. The pharmacodynamics mechanism of FT is determined by means of down-regulating AD-associated cytokines (IL-4, IL-5, IL-22, IL-33, and TSLP) and up-regulating TGF-β1 level. Moreover, FT can regulate systemic immunity by enhancing tolerogenic dendritic cells (Tol-DCs) to activate regulatory T cells (Treg) differentiation and to decrease the population of Th22 and memory B cells. Overall, topical application of FT is able to enhance Treg secreting TGF-β1 and to down-regulate Th2 cell-mediated immunity so that AD symptoms are significantly alleviated. Thereby, FT is an ideal drug candidate potentially replacing or complementing corticosteroids to be developed and used as a therapeutic agent to treat AD.

The aberrant and constitutive activation of the HOXA cluster genes and the their-co-factor MEIS1 (HOX/MEIS) is a recurrent feature in several types of myeloid and lymphoid leukemias. Aberrant HOX/MEIS expression has been shown to drive limitless leukemia stem cell self-renewal and is therefore an attractive target for therapy in acute myeloid leukemia (AML). However, since HOX/MEIS genes encode DNA-binding transcription factors, small molecules targeting these proteins directly are lacking. Furthermore, targeting the HOX/MEIS network is complicated by the fact that these genes are coordinately regulated and have redundant functions in sustaining leukemic self-renewal. One way of therapeutically targeting aberrant HOX/MEIS transcription is the identification and pharmacologic inhibition of upstream chromatin regulators that coordinately modulate their expression. In order to identify such chromatin regulators, we made use of an endogenous GFP reporter knocked-in to the MEIS1 locus in the high HOX/MEIS-expressing U937 human AML cell line. Using this system, we first performed a high-throughput flow-cytometry-based small-molecule inhibitor screen with a library of 261 compounds targeting epigenetic regulators. In our screen, the most potent hits that reproducibly showed >50% MEIS1-GFP inhibition were small molecules that targeted DOT1L, the histone methyltransferase. DOT1L inhibitors have already been well-characterized as HOX/MEIS regulators and most epigenetic regulators are not targeted by existing compound libraries. Therefore, we decided to use a genetic screening approach to more extensively interrogate the landscape of epigenetic regulators of HOX/MEIS expression in AML. For this, we designed a custom computational pipeline and built a CRISPR library of 10,000 sgRNAs targeting functionally conserved protein domains of all catalogued chromatin modulatory proteins (> 600 proteins - 5 sgRNAs per conserved domain). This list of epigenetic regulators included histone modifying enzymes, chromatin readers, nucleosome remodelers, adaptor proteins and proteins involved in DNA and RNA modifications, as well as other transcriptional regulators. Using this comprehensive, domain-focused CRISPR library, we conducted a phenotypic enrichment screen. Specifically, we used flow cytometry to purify the top 20% GFP-MEIS1 (high) and bottom 20% GFP-MEIS1 (low) expressing cells and identified sgRNAs that were enriched particularly in the GFP-MEIS1 -low vs -high fraction using next generation sequencing. Given the extent and complexity of the CRISPR library, our approach uncovered members of six distinct chromatin modifying complexes as MEIS1 regulators (MAGeCKFlute pipeline, 2 SD > mean) and we could validate > 10 of these hits as bonafide regulators of MEIS1 as well as HOXA genes. We also demonstrated their essentiality for the proliferation of HOX-driven AML cells using arrayed sgRNA competition assays. These validated hits included several known as well as novel chromatin readers and writers amenable to small-molecule targeting. We focused our attention on the KAT7/JADE3 complex and the casein kinase 2 (CK2) family that we validated as potent and selective regulators of HOX/MEIS expression in AML cells. Our studies demonstrated that genetic depletion of components of the KAT7 complex or of the CK2 family could reverse HOX/MEIS activation in human AML cells, leading to a progressive loss of proliferative potential. Importantly, the use of the clinical-grade CK2 inhibitor CX4945 (Silmitasertib) caused a concentration-dependent down-regulation of HOX/MEIS expression in models of HOX-driven AML, leading to significant anti-leukemia effects. Our study provides a framework for the multiplexed identification of actionable dependencies targeting therapeutically recalcitrant oncogenic networks in cancer. Specifically for AML, since Silmitasertib is in Phase 2 trials for treatment of other cancers, our studies may solve the long-standing problem of targeting leukemia stem cells in AML potentially overcoming therapy refractoriness in this devastating disease. Disclosures No relevant conflicts of interest to declare.

It is known that the inertia wheel inverted pendulum (IWIP) is a nonlinear underactuated system. Since the unavoidable friction or unclear interference of the IWIP system, designing a controller for the IWIP is a challenging task. In this paper, a fuzzy-based hybrid control (FBHC) is proposed to make the IWIP system can be stably balanced around the upright position. The FBHC system is comprised of a feedback linearization controller, a fuzzy logic controller and a speed compensated controller. The feedback linearization controller with a fuzzy logic controller can control the priority parameter at the non-actuated joint; however, it does not ensure the control of the inertia wheel speed. The speed compensated controller is designed to stabilize the speed of the inertia wheel once the body angle is stable. Thus, the IWIP system can be stably balanced around the upright position and the disk speed is gradually reduced. Finally, the experimental results are verified that the proposed FBHC can achieve a good dynamic balance effect for the IWIP system, even when there is an external force to push the IWIP system.

PT-peptide is derived from the anti-lipopolysaccharide factor of the swimming crab Portunus trituberculatus. The peptide, consisting of 34 amino acids, contains a lipopolysaccharide binding domain. In this study, we investigated the effect of PT-peptide encapsulated in raw milk-derived extracellular vesicles (EVs), designated as EVs-PT peptide, on immune regulation. The results showed that raw milk-derived EVs efficaciously delivered the PT-peptide into monocytes and elevated immune activity, including reactive oxygen species level, superoxide anion production, and phagocytosis. PT-peptide and EVs-PT peptide also elevated the secretion of cytokines, such as interferon-&gamma, interleukin-6, and tumor necrosis factor-&alpha, in human monocytic THP-1 cells. These results suggest that the PT-peptide could be developed as an immune stimulator.

A subset of acute myeloid and lymphoid leukemia cases harbor a t(10;11)(p13;q14) translocation resulting in the CALM-AF10 fusion gene. Standard chemotherapeutic strategies are often ineffective in treating patients with CALM-AF10 fusions. Hence, there is an urgent need to identify molecular pathways dysregulated in CALM-AF10-positive leukemias which may lay the foundation for novel targeted therapies. Here we demonstrate that the Polycomb Repressive Complex 1 gene BMI1 is consistently overexpressed in adult and pediatric CALM-AF10-positive leukemias. We demonstrate that genetic Bmi1 depletion abrogates CALM-AF10-mediated transformation of murine hematopoietic stem and progenitor cells (HSPCs). Furthermore, CALM-AF10-positive murine and human AML cells are sensitive to the small-molecule BMI1 inhibitor PTC-209 as well as to PTC-596, a compound in clinical development that has been shown to result in downstream degradation of BMI1 protein. PTC-596 significantly prolongs survival of mice injected with a human CALM-AF10 cell line in a xenograft assay. In summary, these results validate BMI1 as a bona fide candidate for therapeutic targeting in AML with CALM-AF10 rearrangements.

A subset of acute myeloid and lymphoid leukemia cases harbor a t(10;11)(p13;q14) translocation resulting in the CALM-AF10 fusion gene. Standard chemotherapeutic strategies are often ineffective in treating patients with CALM-AF10 fusions. Hence, there is an urgent need to identify molecular pathways dysregulated in CALM-AF10-positive leukemias which may lay the foundation for novel targeted therapies. Here we demonstrate that the Polycomb Repressive Complex 1 geneBMI1is consistently overexpressed in adult and pediatric CALM-AF10-positive leukemias. We demonstrate that geneticBmi1depletion abrogates CALM-AF10-mediated transformation of murine hematopoietic stem and progenitor cells (HSPCs). Furthermore, CALM-AF10-positive murine and human AML cells are profoundly sensitive to the small-molecule BMI1 inhibitor PTC209 as well as to PTC596, a compound in clinical development that has been shown to result in downstream degradation of BMI1 protein. PTC-596 significantly prolongs survival of mice injected with a human CALM-AF10 cell line in a xenograft assay. In summary, these results validate BMI1 as abonafidecandidate for therapeutic targeting in AML with CALM-AF10 rearrangements.

Gene perturbation studies have been extensively used to investigate the role of individual genes in AML pathogenesis. For achieving complete gene disruption, many of these studies have made use of complex gene knockout models. While these studies with knockout mice offer an elegant and time-tested system for investigating genotype-to-phenotype relationships, a rapid and scalable method for assessing candidate genes that play a role in AML cell proliferation or survival in AML models will help accelerate the parallel interrogation of multiple candidate genes. Recent advances in genome-editing technologies have dramatically enhanced our ability to perform genetic perturbations at an unprecedented scale. One such system of genome editing is the CRISPR-Cas9-based method that can be used to make rapid and efficacious alterations in the target cell genome. The ease and scalability of CRISPR/Cas9-mediated gene-deletion makes it one of the most attractive techniques for the interrogation of a large number of genes in phenotypic assays. Here, we present a simple assay using CRISPR/Cas9 mediated gene-disruption combined with high-throughput flow-cytometry-based competition assays to investigate the role of genes that may play an important role in the proliferation or survival of human and murine AML cell lines.

In recent years, artificial intelligence has developed rapidly, and robots have become the object of research and development. The robots can be seen in various exhibition venues or public places. This paper proposes a customer service system on robots for pharmacy. The system includes question and answer and multimedia feedback about pharmacy. The whole system is divided into two parts. One is the expert system for pharmacy, the other is multimedia feedback. The expert system we designed includes health knowledge question and answer, product location, special disease related issues, etc. We uses the question and answer method to present these functions, obtain the highest similarity score through the similarity calculation, and then search for the knowledge base answer and the result is passed back to the user. The other part is the multimedia feedback function, which has many functions related to the pharmacy in the system. Through these feedbacks, you can understand the current operation status of the pharmacy or related activities.

This paper proposes and presents the experimental demonstration of 320-Gb/s free-space optical (FSO) communication based on dense-wavelength-division-multiplexing (DWDM) technology and afocal scheme. To the best of our knowledge, this is the first one that adopts DWDM technology and afocal scheme to successfully demonstrate 50-m/320-Gb/s FSO communication. Results show that the free-space transmission distance is greatly increased by the afocal scheme and that the free-space transmission rate is significantly enhanced by the DWDM technology. DWDM FSO communication over a 50-m free-space link with a total transmission rate of 320 Gb/s $(40\;\text{Gb/s}/\lambda \times 8\lambda=320\;\text{Gb/s})$ is achieved. With the aid of a low-noise amplifier and clock/data recovery at the receiving site, good bit-error-rate (BER) performance and clear eye diagram are obtained at a 50-m/320-Gb/s operation. Such 50-m/320-Gb/s DWDM FSO communication provides the advantages of optical wireless communications for long transmission distance and high transmission rate, which is thoroughly useful for long-haul and high-speed light-based WiFi (LiFi) applications.

Fiber-wireless and fiber-invisible laser light communication (IVLLC) convergences that adopt the Mach–Zehnder modulator-optoelectronic oscillator (MZM-OEO)-based broadband light source for microwave (MW)/millimeter-wave (MMW)/baseband (BB) signal transmission are proposed and demonstrated. For downlink transmission, light is optically promoted from 15- and 25-GHz radio-frequency (RF) signals to 10-Gb/s/30-GHz MW, 15-Gb/s/50-GHz MMW, 20-Gb/s/60-GHz MMW, and 25-Gb/s/100-GHz MMW data signals based on fiber-wireless and fiber-IVLLC integrations. Bit error rate (BER) performs efficiently in the 40-km single-mode fiber (SMF) and the 10-m RF/25-m optical wireless transport scenarios. For uplink transmission, downstream light is successfully intensity-modulated with a 25-Gb/s BB data stream based on fiber-IVLLC integration. BER performs efficiently in the 40-km SMF and the 100-m optical wireless transport scenario. Such a hybrid MW/MMW/BB lightwave transmission system is an attractive alternative. It is shown to be a prominent one to present advancements in integrating fiber backbone and radio-frequency (RF)/optical wireless feeder networks.

The importance of epigenetic dysregulation to acute myeloid leukemia (AML) pathophysiology has become increasingly apparent in recent years. Epigenetic regulators, including readers, writers, and erasers, are recurrently dysregulated by way of chromosomal translocations, somatic mutations, or genomic amplification in AML and many of these alterations are directly implicated in AML pathogenesis. Mutations in epigenetic regulators are often discovered in founder clones and persist after therapy, indicating that they may contribute to a premalignant state poised for the acquisition of cooperating mutations and frank malignancy. Apart from the proto-oncogenic impact of these mutations, the AML epigenome is also shaped by other epigenetic factors that are not mutated but co-opted by AML oncogenes, presenting with actionable vulnerabilities in this disease. Targeting the AML epigenome might also be important for eradicating AML leukemia stem cells, which can be critical for disease maintenance and resistance to therapy. In this review, we describe the importance of epigenetic regulators in AML. We also summarize evidence implicating specific epigenetic regulators in AML pathobiology and discuss emerging epigenome-based therapies for the treatment of AML in the clinic.

Mitochondrial function is applied as oxidative stress and neuronal damage index. In this study, d-galactose was used to induce free radicals production and neuronal damage in HN-h cells, and the effect of novel 43 kDa protein isolated from oyster on anti-mitochondrial dysfunction and zinc-binding ability were evaluated. Crystal violet stain results indicated zinc-binding protein of oyster (ZPO) attenuated neuronal cell death induced by 100 mM of d-galactose on HN-h cells in a dose-dependent manner. ZPO alleviated mitochondrial inactivation, mitochondrial membrane potential decreasing, oxidative stress, and fusion/fission state in non-cytotoxic concentration of d-galactose (50 mM)-treated HN-h cells. ZPO treatment recovered metallathionein-3 (MT-3) decrease and inhibited β- and γ-secretase as well as amyloid beta (Aβ) accumulation in HN-h cells caused by d-galactose induction. These results suggest ZPO could avoid oxidative stress and is a functional protein for zinc concentration maintainability, which has potential for development of functional foods for neuronal protection.

This study proposes and presents the experimental demonstration of a 320 Gbps free-space optical (FSO) communication based on dense-wavelength-division-multiplexing (DWDM) technology and afocal scheme. Good bit error rate (BER) performance and clear eye diagram are obtained at a 50 m/320 Gbps operation.

Fiber-wireless and fiber-invisible laser light communication (IVLLC) convergences that adopt Mach-Zehnder modulator (MZM)-optoelectronic oscillator (OEO)-based broadband light source (BLS) for microwave (MW)/millimeter-wave (MMW)/baseband (BB) signal transmission is proposed and experimentally demonstrated.