Level of empowerment of hospitalized patient in Taiwan clinical practice.

PURPOSE: In the health-care system within hospitals, Taiwanese patients usually play the role of passively cooperating with health-care professionals. Therefore, patients rarely make their own treatment decisions. This study evaluated the level of patient education and patient satisfaction in relation to empowerment level in Taiwan. METHODS: A cross-sectional survey by a self-administered structured questionnaire was carried out with 618 inpatients from the four hospitals. Statistical analyses were then conducted. Analysis of covariance and post-hoc comparison was used to compare differences between the level of patient empowerment, age, and education as covariates in the model. RESULTS: This study found that 21.2% and 35.6% of participants were highly empowered and well empowered, respectively. Years of education is a significant covariate in the counselling domain of patient education. Even after controlling for age and education level, the counselling, answer question and justifying action, providing information scores remain significant for all levels after adjusting for the effects of degree of patient empowerment. Patients with higher empowerment also having more-sufficient patient education, indicating a tendency toward higher patient satisfaction. Patient education and counselling practices in Taiwan's clinical practice could be improved to enhance patient empowerment and ensure health-care systems are person-centred. CONCLUSIONS: To move more toward highly patient empowerment, we suggest that health-care professionals advocate a patient-empowerment approach and to provide more counselling related to patients' illnesses and possible treatments.

Icaritin Derivative IC2 Induces Cytoprotective Autophagy of Breast Cancer Cells via SCD1 Inhibition.

Breast cancer is one of the most prevalent malignancies and the leading cause of cancer-associated mortality in China. Icaritin (ICT), a prenyl flavonoid derived from the Epimedium Genus, has been proven to inhibit the proliferation and stemness of breast cancer cells. Our previous study demonstrated that IC2, a derivative of ICT, could induce breast cancer cell apoptosis by Stearoyl-CoA desaturase 1 (SCD1) inhibition. The present study further investigated the mechanism of the inhibitory effects of IC2 on breast cancer cells in vitro and in vivo. Our results proved that IC2 could stimulate autophagy in breast cancer cells with the activation of adenosine monophosphate (AMP)-activated protein kinase (AMPK) signaling and mitogen-activated protein kinase (MAPK) signaling. Combination treatment of the AMPK inhibitor decreased IC2-induced autophagy while it markedly enhanced IC2-induced apoptosis. In common with IC2-induced apoptosis, SCD1 overexpression or the addition of exogenous oleic acid (OA) could also alleviate IC2-induced autophagy. In vivo assays additionally demonstrated that IC2 treatment markedly inhibited tumor growth in a mouse breast cancer xenograft model. Overall, our study was the first to demonstrate that IC2 induced cytoprotective autophagy by SCD1 inhibition in breast cancer cells and that the autophagy inhibitor markedly enhanced the anticancer activity of IC2. Therefore, IC2 was a potential candidate compound in combination therapy for breast cancer.

Identification of icaritin derivative IC2 as an SCD-1 inhibitor with anti-breast cancer properties through induction of cell apoptosis.

BACKGROUND: Breast cancer is the most common malignancy affecting women, yet effective targets and related candidate compounds for breast cancer treatment are still lacking. The lipogenic enzyme, stearoyl-CoA desaturase-1 (SCD1), has been considered a potential target for breast cancer treatment. Icaritin (ICT), a prenylflavonoid derivative from the Traditional Chinese Medicine Epimedii Herba, has been reported to exert anticancer effects in various types of cancer. The purpose of the present study was to explore the effect of the new ICT derivative, IC2, targeting SCD1 on breast cancer cells and to explore the specific mechanism. METHODS: Immunohistochemistry and semiquantitative evaluation were performed to detect the expression level of SCD1 in normal and tumor samples. Computer-aided drug design (CADD) technology was used to target SCD1 by molecular docking simulation, and several new ICT derivatives were prepared by conventional chemical synthesis. Cell viability was evaluated by an MTT assay and dead cell staining. SCD1 expression in cancer cells was determined by Western blot and qRT-PCR analyses. The enzymatic activity of SCD1 was evaluated by detecting the conversion rate of [d31] palmitic acid (PA) using Gas chromatography-mass spectrometry (GC-MS). DAPI staining, flow cytometry and Western blot were used to detect cell apoptosis. Mitochondrial membrane potential and reactive oxygen species (ROS) assays were used to determine cell mitochondrial function. Lentiviral transduction was utilized to generate SCD1-overexpressing cell lines. RESULTS: We found that SCD1 was overexpressed and correlated with poor prognosis in breast cancer patients. Among a series of ICT derivatives, in vitro data showed that IC2 potentially inhibited the viability of breast cancer cells, and the mechanistic study revealed that IC2 treatment resulted in ROS activation and cellular apoptosis. We demonstrated that IC2 inhibited SCD1 activity and expression in breast cancer cells in a dose-dependent manner. Moreover, SCD1 overexpression alleviated IC2-induced cytotoxicity and apoptosis in breast cancer cells. CONCLUSIONS: The new ICT derivative, IC2, was developed to induce breast cancer cell apoptosis by inhibiting SCD1, which provides a basis for the development of IC2 as a potential clinical compound for breast cancer treatment.

Resource allocation algorithm of an indoor OFDMA VLC system.

In this work, a resource management algorithm is proposed for an indoor visible light communication (VLC) access network using an orthogonal frequency division multiple access (OFDMA) scheme. With OFDMA, adaptive modulation is adopted to improve the frequency spectrum efficiency of this VLC system. Specifically, the long-term time-averaged optimization problem is transformed into a series of single timeslot online problems via a Lyapunov optimization technique. Then, each user is provided with a separate queue to maintain the random arrival data by a VLC access point, and a subcarrier allocation solution is subsequently presented to maximize the transmission rate. Numerical simulation shows that compared with the best channel state information (BC) algorithm and round robin (RR) algorithm, the proposed algorithm can not only ensure the transmission rate but also greatly improve system stability. In particular, for mean arrival rate B=7Kbits/timeslot, the system stability by the proposed algorithm improves by about 53.36% and 61.36% in comparison with BC and RR algorithms, respectively. This work will benefit the design and development of indoor OFDMA VLC systems.

Transmission rate Optimization by dynamic resource allocation algorithm for RF/VLC heterogeneous networks.

In this work, a dynamic resource allocation (DRA) algorithm is proposed to optimize the transmission rate subject to the access point assignment, bandwidth and transmit power allocation in RF/VLC heterogeneous networks, which combines the visible light communication (VLC) access point (AP) and radio frequency (RF) AP. To optimize the allocation among resource block (RB), subchannel and power, the time-average transmission rate is maximized under time-average transmit power budget. Specifically, the time-average optimization problem is converted into series of single timeslot online problem by Lyapunov optimization technique. Because of its complexity and non-convexity, the problem is decomposed into three independent subproblems for which a non-iterative solution is presented on the basis of Lagrange relaxation and convex optimization theory. Numerical simulations are conducted to demonstrate the effectiveness of the proposed DRA algorithm. And the comparisons with two classical algorithms are also given in terms of transmission rate and system stability. This work will benefit the design and development of hybrid RF/VLC system.

Melatonin exerts neuroprotective effects by inhibiting neuronal pyroptosis and autophagy in STZ-induced diabetic mice.

Diabetes mellitus (DM) patients are at a higher risk of developing brain injury characterized by neuronal death. Melatonin, a hormone produced by the pineal gland, exerts neuroprotective effects against brain damage. However, the effect of melatonin on diabetes-induced brain injury has not been elucidated. This study was to evaluate the role of melatonin against neuronal death in DM and to elucidate the underlying mechanisms. Herein, we found that melatonin administration significantly alleviated the neuronal death in both streptozotocin (STZ)-induced diabetic mice and high glucose (HG)-treated neuronal cells. Melatonin inhibited neuronal pyroptosis and excessive autophagy, as evidenced by decreased levels of NLRP3, cleaved caspase-1, GSDMD-N, IL-1ß, LC3, Beclin1, and ATG12 both in vivo and in vitro. MicroRNA-214-3p (miR-214-3p) was decreased in DM mice and HG-treated cells, and such a downregulation was corrected by melatonin, which was accompanied by repression of caspase-1 and ATG12. Furthermore, downregulation of miR-214-3p abrogated the anti-pyroptotic and anti-autophagic actions of melatonin in vitro. Our results indicate that melatonin exhibits a neuroprotective effect by inhibiting neuronal pyroptosis and excessive autophagy through modulating the miR-214-3p/caspase-1 and miR-214-3p/ATG12 axes, respectively, and it might be a potential agent for the treatment of brain damage in the setting of DM.

Melatonin alleviates cardiac fibrosis via inhibiting lncRNA MALAT1/miR-141-mediated NLRP3 inflammasome and TGF-ß1/Smads signaling in diabetic cardiomyopathy.

Melatonin is a hormone produced by the pineal gland, and it has extensive beneficial effects on various tissue and organs; however, whether melatonin has any effect on cardiac fibrosis in the pathogenesis of diabetic cardiomyopathy (DCM) is still unknown. Herein, we found that melatonin administration significantly ameliorated cardiac dysfunction and reduced collagen production by inhibiting TGF-ß1/Smads signaling and NLRP3 inflammasome activation, as manifested by downregulating the expression of TGF-ß1, p-Smad2, p-Smad3, NLRP3, ASC, cleaved caspase-1, mature IL-1ß, and IL-18 in the heart of melatonin-treated mice with diabetes mellitus (DM). Similar beneficial effects of melatonin were consistently observed in high glucose (HG)-treated cardiac fibroblasts (CFs). Moreover, we also found that lncRNA MALAT1 (lncR-MALAT1) was increased along with concomitant decrease in microRNA-141 (miR-141) in DM mice and HG-treated CFs. Furthermore, we established NLRP3 and TGF-ß1 as target genes of miR-141 and lncR-MALAT1 as an endogenous sponge or ceRNA to limit the functional availability of miR-141. Finally, we observed that knockdown of miR-141 abrogated anti-fibrosis action of melatonin in HG-treated CFs. Our findings indicate that melatonin produces an antifibrotic effect via inhibiting lncR-MALAT1/miR-141-mediated NLRP3 inflammasome activation and TGF-ß1/Smads signaling, and it might be considered a potential agent for the treatment of DCM.

Uniformity improvement on received optical power for an indoor visible light communication system with an angle diversity receiver.

In this work, an angle diversity receiver (ADR) structure is proposed to optimize the uniformity of the received optical power distribution in an indoor visible light communication (VLC) system. Taking the rectangular and hybrid layouts with 16 light-emitting diodes as examples, different inclination angles and the number of side detectors are investigated with three diversity combining techniques in a typical room, where the primary reflection of the wall is considered. Simulation results showed that the inclination angles and the number of side detectors would affect the variance and average of the received optical power, and the variance would decrease with the increase of the number of side detectors. In addition, maximal ratio combining is more suitable for the ADR when the variance and average of the received optical power are considered simultaneously. By applying the ADR with five side detectors, the variances of the received optical power will decrease by 81.34% and 86.09% under the rectangle layout and the hybrid layout, respectively. This work will benefit the design and development of the VLC system.

Bmi deficiency causes oxidative stress and intervertebral disc degeneration which can be alleviated by antioxidant treatment.

The transcriptional repressor Bmi-1 is involved in cell-cycle regulation and cell senescence, the deficiency of which has been shown to cause oxidative stress. This study investigated whether Bmi-1 deficiency plays a role in promoting disc degeneration and the effect of treatment with antioxidant N-acetylcysteine (NAC) on intervertebral disc degeneration. Bmi-1-/- mice were treated with the antioxidant NAC, supplied in drinking water (Bmi-1-/- +NAC). For in vitro experiments, mouse intervertebral discs were cultured under low oxygen tension and serum-limiting conditions in the presence of tumour necrosis factor α and interleukin 1ß in order to mimic degenerative insult. Disc metabolism parameters in these in vitro and in vivo studies were evaluated by histopathological, immunohistochemical and molecular methods. Bmi-1-/- mice showed lower collagen Ⅱ and aggrecan levels and higher collagen Ⅹ levels than wild-type and Bmi-1-/- +NAC mice. Bmi-1-/- mice showed significantly lower superoxide dismutase (SOD)-1, SOD-2, glutathione peroxidase (GPX)-1 and GPX-3 levels than their wild-type littermates and Bmi-1-/- + NAC mice. Relative to Bmi-1-/- mice, the control and Bmi-1-/- +NAC mice showed significantly lower p16, p21, and p53 levels. These results demonstrate that Bmi-1 plays an important role in attenuating intervertebral disc degeneration in mice by inhibiting oxidative stress and cell apoptosis.

Inhibition of microRNA-150-5p alleviates cardiac inflammation and fibrosis via targeting Smad7 in high glucose-treated cardiac fibroblasts.

Hyperglycemia-induced cardiac fibrosis is a prominent characteristic of diabetic cardiomyopathy. Changes in proinflammatory cytokines have been shown to lead to cardiac fibrosis in patients with diabetes mellitus. This study aimed to investigate the role of miR-150-5p in mediating cardiac inflammation and fibrosis in cardiac fibroblasts (CFs). Herein, we found that high-glucose (HG) treatment significantly induced cardiac inflammation, as manifested by increased proinflammatory cytokine production (IL-1ß) and NF-κB activity in CFs. Moreover, HG markedly aggravated cardiac fibrosis and increased levels of fibrotic markers (CTGF, FN, α-SMA) and extracellular matrix proteins (Col-I, Col-III) in CFs. At the same time, HG disturbed the TGF-ß1/Smad signaling pathway, as evidenced by increases in TGF-ß1 and p-Smad2/3 levels and decreases in Smad7 levels in CFs. Furthermore, we found that miR-150-5p was upregulated by HG, which negatively regulated Smad7 expression at the posttranscription level. Further study demonstrated that cardiac inflammation and fibrosis in CFs were corrected following miR-150-5p knockdown, but exacerbated by miR-150-5p overexpression. These data indicated that miR-150-5p inhibition could ameliorate NF-κB-related inflammation and TGF-ß1/Smad-induced cardiac fibrosis through targeting Smad7. Thus, miR-150-5p may be a novel promising target for treating diabetic cardiomyopathy.

Optimized design of the light source for an indoor visible light communication system based on an improved bat algorithm.

Aiming at the problem of uneven distribution of receiving illuminance and optical power on the receiving plane of the visible light communication (VLC) system, this paper proposes a light source optimization method based on an improved bat algorithm (IBA). Taking the rectangular and hybrid layouts with 16 light-emitting diodes (LEDs), as examples, we set the variance of received light power on the receiving plane as the fitness function. By redesigning the speed update method and local search method of the traditional bat algorithm (BA), the IBA is used to optimize the LED half-power angle and LED position that affect the system performance. The simulation results show that, considering the primary reflection of the wall, the method can reduce the received illumination and optical power fluctuation of the receiving plane within a limited number of iterations under different light source layout schemes.

A novel heterozygous intron mutation in SEMA7A causing kallmann syndrome in a female.

Kallmann syndrome (KS) is a rare inherited disorder, which has significantly genotypic and phenotypic heterogeneity. KS is clinically characterized by the combination of hypogonadotropic hypogonadism and hypo/anosmia. At present, there is no relevant report that intron mutation in SEMA7A gene helps induce KS. A 17-year-old Chinese female (46, XX) came to our department due to primary amenorrhea, who actually had hyposmia since her childhood. Hypogonadotropic hypogonadism was then detected. Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels were remarkably low. And estradiol level was extremely low. The laboratory test results were consistent with KS. A heterozygous point mutation of intron 13 in SEMA7A (NM_003612.3:c.1640-3C > A) was identified. The patient received the treatment of pulsatile gonadotropin-releasing hormone (GnRH) pump, which could imitate physiological ovarian stimulation, thus resulting in mature follicle and a peak of LH. The patient was injected subcutaneously every 90 min with a dose of 10 µg per pulse, which had bona efficacy. She acquired menarche at about 43 days after the treatment. We firstly report a case of KS caused by a novel mutation site in the intron of SEMA7A gene. We mainly provide insight into the clinical manifestations, genetic diagnosis and treatment of KS.

miR-150 regulates glucose utilization through targeting GLUT4 in insulin-resistant cardiomyocytes.

MicroRNAs (miRNAs) play an important role in cardiac function and metabolism. However, whether they regulate insulin resistance (IR) of cardiomyocytes remains unclear. The aim of the present study was to shed light on this issue with a focus on miR-150. We found here that miR-150 level was elevated in myocardium of type 2 diabetes mellitus (T2DM) rat model and in insulin-resistant cardiomyocytes induced by high glucose (25 mM) and high insulin (1 µM). Deregulation of miR-150 downregulated the protein and mRNA levels of glucose transporter 4 (GLUT4) as assessed by western blot, real-time polymerase chain reaction (qPCR), and immunofluorescence assays. Overexpression of miR-150 inhibited glucose utilization in cardiomyocytes as detected by 2-deoxyglucose transport and glucose consumption assays. In contrast, knockdown of miR-150 significantly increased glucose uptake in cardiomyocytes. Moreover, GLUT4 translocation was increased after transfection of miR-150 inhibitor (AMO-150). Collectively, miR-150 reduced glucose utilization by directly decreasing the expression and translocation of GLUT4 in the cardiomyocytes with IR and therefore might be a new therapeutic target for metabolic diseases such as T2DM.

Silymarin ameliorates diabetic cardiomyopathy via inhibiting TGF-ß1/Smad signaling.

Diabetic cardiomyopathy (DCM) is the leading cause of morbidity and mortality in diabetes mellitus (DM) patients. Previous studies have shown that the transforming growth factor-beta 1 (TGF-ß1)/Smad signaling pathway plays a key role in the development of myocardial fibrosis in DCM. Silymarin (SMN) is used clinically to treat liver disorders and acts by influencing TGF-ß1. However, the possible effects of silymarin on DCM remain to be elucidated. In our study, the DM animal model was induced by streptozotocin (STZ) injection. Fasting blood glucose level was measured, and the structure and function of the heart were measured by hematoxylin and eosin (H&E) and Masson staining, echocardiography, and transmission electron microscopy (TEM). Western blot was used to detect the expression of TGF-ß1, Smad2/3, phosphorylation Smad2/3(p-Smad2/3), and Smad7. Our results showed that silymarin downregulated blood glucose level and significantly improved cardiac fibrosis and collagen deposition in DM rats detected by H&E, Masson staining, and TEM assays. The echocardiography results showed that silymarin administration attenuated cardiac dysfunction in DM rats. Additionally, compared with untreated DM rats, levels of TGF-ß1 and p-Smad2/3 were decreased, whereas Smad7 was increased following silymarin administration. These data demonstrate that silymarin ameliorates DCM through the inhibition of TGF-ß1/Smad signaling, suggesting that silymarin may be a potential target for DCM treatment.

Exploiting dimensionality and defect mitigation to create tunable microwave dielectrics.

The miniaturization and integration of frequency-agile microwave circuits--relevant to electronically tunable filters, antennas, resonators and phase shifters--with microelectronics offers tantalizing device possibilities, yet requires thin films whose dielectric constant at gigahertz frequencies can be tuned by applying a quasi-static electric field. Appropriate systems such as BaxSr1-xTiO3 have a paraelectric-ferroelectric transition just below ambient temperature, providing high tunability. Unfortunately, such films suffer significant losses arising from defects. Recognizing that progress is stymied by dielectric loss, we start with a system with exceptionally low loss--Srn+1TinO3n+1 phases--in which (SrO)2 crystallographic shear planes provide an alternative to the formation of point defects for accommodating non-stoichiometry. Here we report the experimental realization of a highly tunable ground state arising from the emergence of a local ferroelectric instability in biaxially strained Srn+1TinO3n+1 phases with n ≥ 3 at frequencies up to 125 GHz. In contrast to traditional methods of modifying ferroelectrics-doping or strain-in this unique system an increase in the separation between the (SrO)2 planes, which can be achieved by changing n, bolsters the local ferroelectric instability. This new control parameter, n, can be exploited to achieve a figure of merit at room temperature that rivals all known tunable microwave dielectrics.

Coriolus versicolor alleviates diabetic cardiomyopathy by inhibiting cardiac fibrosis and NLRP3 inflammasome activation.

Coriolus versicolor (CV) is a traditional medicine and food mushroom. Our previous study demonstrated that CV extract exhibited anti-hyperglycemia and anti-insulin resistance effects. However, the effect of CV on cardiac function in diabetic cardiomyopathy (DCM) remains unclear. Therefore, we aimed to investigate the effect of CV on cardiac function in diabetes mellitus (DM) rats. We found that the cardiac dysfunction of DM rats was markedly improved by CV extract treatment. CV extract administration significantly attenuated cardiac fibrosis in DM rats, which was accompanied by suppressed transforming growth factor beta 1 (TGF-ß1)/Smad signaling as indicated by decreased levels of TGF-ß1, p-Smad2, and p-Smad3 and increased Smad7 expression. Moreover, CV extract treatment significantly alleviated cardiac inflammation as shown by decreased levels of NLRP3 receptor, cleaved caspase-1, IL-1ß, and IL-18 in DM rats at least partly due to the inhibition of the NF-κB. In addition, high-glucose treatment induced cardiac fibrosis and increased cardiac inflammation in cardiac fibroblast cells, but these effects were ameliorated by CV extract treatment. Therefore, we conclude that the protective effect of CV on DCM is associated with the suppression of TGF-ß1/Smad signaling and attenuation of NLRP3 inflammasome activation, suggesting that CV extract may be a potential therapeutic agent for DCM.

Bradykinin-mediated Ca2+ signalling regulates cell growth and mobility in human cardiac c-Kit+ progenitor cells.

Our recent study showed that bradykinin increases cell cycling progression and migration of human cardiac c-Kit+ progenitor cells by activating pAkt and pERK1/2 signals. This study investigated whether bradykinin-mediated Ca2+ signalling participates in regulating cellular functions in cultured human cardiac c-Kit+ progenitor cells using laser scanning confocal microscopy and biochemical approaches. It was found that bradykinin increased cytosolic free Ca2+ ( Cai2+ ) by triggering a transient Ca2+ release from ER IP3Rs followed by sustained Ca2+ influx through store-operated Ca2+ entry (SOCE) channel. Blockade of B2 receptor with HOE140 or IP3Rs with araguspongin B or silencing IP3R3 with siRNA abolished both Ca2+ release and Ca2+ influx. It is interesting to note that the bradykinin-induced cell cycle progression and migration were not observed in cells with siRNA-silenced IP3R3 or the SOCE component TRPC1, Orai1 or STIM1. Also the bradykinin-induced increase in pAkt and pERK1/2 as well as cyclin D1 was reduced in these cells. These results demonstrate for the first time that bradykinin-mediated increase in free Cai2+ via ER-IP3R3 Ca2+ release followed by Ca2+ influx through SOCE channel plays a crucial role in regulating cell growth and migration via activating pAkt, pERK1/2 and cyclin D1 in human cardiac c-Kit+ progenitor cells.

LncRNA KCNQ1OT1 Mediates Pyroptosis in Diabetic Cardiomyopathy.

BACKGROUND/AIMS: Diabetic cardiomyopathy (DCM) is a common complication of diabetes and can cause heart failure, arrhythmia and sudden death. The pathogenesis of DCM includes altered metabolism, mitochondrial dysfunction, oxidative stress, inflammation, cell death and extracellular matrix remodeling. Recently, pyroptosis, a type of programmed cell death related to inflammation, was proven to be activated in DCM. However, the molecular mechanisms underlying pyroptosis in DCM remain elusive. The long non-coding RNA (lncRNA) Kcnq1ot1 participates in many cardiovascular diseases. This study aims to clarify whether Kcnq1ot1 affects cardiac pyroptosis in DCM. METHODS: AC16 cells and primary cardiomyocytes were incubated with 5.5 and 50 mmol/L glucose. Diabetic mice were induced with streptozotocin (STZ). Kcnq1ot1 was silenced both in vitro and in vivo. qRT-PCR was used to detect the expression level of Kcnq1ot1. Immunofluorescence, qRT-PCR and western blot analyses were used to detect the degree of pyroptosis. Echocardiography, hematoxylin and eosin staining, and Masson's trichrome staining were used to detect the cardiac function and morphology in mice. Cell death and function were detected using TUNEL staining, immunofluorescence staining and Ca2+ measurements. RESULTS: The expression of Kcnq1ot1 was increased in patients with diabetes, high glucose-induced cardiomyocytes and diabetic mouse cardiac tissue. Silencing Kcnq1ot1 alleviated pyroptosis by targeting miR-214-3p and caspase-1. Furthermore, silencing Kcnq1ot1 reduced cell death, cytoskeletal structure abnormalities and calcium overload in vitro and improved cardiac function and morphology in vivo. CONCLUSION: Kcnq1ot1 is overexpressed in DCM, and silencing Kcnq1ot1 inhibits pyroptosis by influencing miR-214-3p and caspase-1 expression. We clarified for the first time that Kcnq1ot1 could be a new therapeutic target for DCM.

Artificial Magnetotaxis of Microbot: Magnetophoresis versus Self-Swimming.

An artificial magnetotactic microbot was created by integrating the microalgal cell with magnetic microbead for its potential application as biomotor in microscale environment. Here, we demonstrate the remote magnetotactic control of the microbot under a low gradient magnetic field (<100 T/m). We characterize the kinematic behavior of the microbots carrying magnetic microbeads of two different sizes, with diameter of 2 and 4.5 µm, in the absence and presence of magnetic field. In the absence of magnetic field, we observed the microbot showed a helical motion as a result of the misalignment between the thrust force and the symmetry axis after the attachment. The microbot bound with a larger magnetic microbead moved with higher translational velocity but rotated slower about its axis of rotation. The viscous force was balanced by the thrust force of the microbot, resulting in a randomized swimming behavior of the microbot at its terminal velocity. Meanwhile, under the influence of a low gradient magnetic field, we demonstrated that the directional control of the microbot was based on following principles: (1) magnetophoretic force was insignificant on influencing its perpendicular motion and (2) its parallel motion was dependent on both self-swimming and magnetophoresis, in which this cooperative effect was a function of separation distance from the magnet. As the microbot approached the magnet, the magnetophoretic force suppressed its self-swimming behavior, leading to a positive magnetotaxis of the microbot toward the source of magnetic field. Our experimental results and kinematic analysis revealed the contribution of mass density variation of particle-and-cell system on influencing its dynamical behavior.

The Relationship Between Liver Enzymes and Insulin Resistance in Type 2 Diabetes Patients with Nonalcoholic Fatty Liver Disease.

Non-: alcoholic fatty liver disease (NAFLD) is prevalent worldwide, especially in patients with type 2 diabetes. Liver enzymes are the main warning signs of liver injury and insulin resistance (IR) is critical to NAFLD. This study was aimed to investigate the association between liver enzymes and insulin resistance in type 2 diabetes patients with NAFLD. Data from 212 diabetes patients with NAFLD were analyzed, including 118 males and 94 females who received care from 2014 to 2015. The patients were divided into three groups by severity (mild n=87, moderate n=89, severe n=36). All patients underwent standard clinical and laboratory examinations. Liver enzymes including alanine aminotransferase (ALT), aspartate aminotransferase (AST), and γ-glutamyl transferase (GGT) were measured, serum fasting glucose and serum fasting insulin were obtained. IR was assessed using the homeostasis model assessment insulin resistance index (HOMA-IR). Age, sex, and BMI did not significantly differ in patients (p>0.05). Compared with normal levels, elevated ALT and AST were associated with a higher HOMA-IR (p=0.0035, p=0.0096, respectively). HOMA-IR did not significantly differ (p>0.05) between patients with normal and elevated GGT. HOMA-IR increased as the levels of liver enzymes increased, and each enzyme showed a significant association with HOMA-IR (p=0.0166, p<0.0001, and p <0.0001). HOMA-IR differs between normal and elevated ALT and AST. Liver enzymes are associated with HOMA-IR in type 2 diabetes patients with NAFLD. These findings can help evaluate the degree of IR and hepatocellular steatosis in patients and prevent the progression of type 2 diabetes and NAFLD in clinical practice.