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We reported the photoconduction properties of tungsten disulfide (WS2) nanoflakes obtained by the mechanical exfoliation method. The photocurrent measurements were carried out using a 532 nm laser source with different illumination powers. The results reveal a linear dependence of photocurrent on the excitation power, and the photoresponsivity shows an independent behavior at higher light intensities (400–4000 Wm−2). The WS2 photodetector exhibits superior performance with responsivity in the range of 36–73 AW−1 and a normalized gain in the range of 3.5–7.3 10−6 cm2V−1 at a lower bias voltage of 1 V. The admirable photoresponse at different light intensities suggests that WS2 nanostructures are of potential as a building block for novel optoelectronic device applications. [ABSTRACT FROM AUTHOR]

We have presented the room-temperature persistent photoconductivity (PPC) effect in γ-InSe layered semiconductors. The PPC effect can be observed in the temperature range from room temperature down to 200 K, and the PPC decay is well described by a stretch-exponential function. The temperature-dependent PPC and performance of PPC decay indicate that the random local-potential fluctuations (RLPF) mechanism is responsible for PPC effect inγ-InSe. In addition, the PPC behavior at different temperature regions can be well explained by the percolation model associated with the RLPF mechanism. • The observed room-temperature persistent photoconductivity in γ-InSe layered semiconductor. • The mechanism of persistent photoconductivity inγ-InSe is attributed to RLPF model. • The PPC behavior with temperature dependence for our sample is explained by percolation model. [ABSTRACT FROM AUTHOR]

Background: Organophosphate flame retardants (OPFRs) are extensively distributed in our environment, prompting concerns about potential health hazards, including lung injuries resulting from OPFR exposure. Methods: The present study recruited 125 lung cancer patients, assessing their exposure to 10 OPFR compounds through urine samples. The final analysis comprised 108 participants after excluding those lacking epidermal growth factor receptor (EGFR) status and those with chronic kidney disease. Demographic and clinical characteristics, as well as urinary OPFR concentrations, were compared based on OPFR detection. Spearman correlation was conducted to explore the relationship between OPFR compounds, while logistic regression was used to identify OPFR compounds associated with EGFR mutation. Results: The study revealed widespread OPFR exposure among lung cancer patients, with an overall detection frequency of 99.07%. Tris(2‐butoxyethyl) phosphate (TBEP) exhibited a strong correlation to its metabolite bis(2‐butoxyethyl) phosphate (r = 0.88, p < 0.01). Patients with TBEP in their urine had higher percentage of wild‐type EGFR and the detection of TBEP was associated with a reduced likelihood of mutant EGFR expression. Conclusions: OPFR exposure was prevalent in lung cancer patients, with TBEP detection identified as a factor with lower EGFR mutation expression. This study contributes to the understanding of OPFR exposure in lung cancer patients and underscores the significance of TBEP in evaluating EGFR mutation in this population. [ABSTRACT FROM AUTHOR]

Background/Aims: Hyperglycemia has been shown to increase the incidence and metastasis in various types of cancers. However, the correlation between hyperglycemia and lymphatic metastasis in prostate cancer (PCa) remains unclear. Our previous study demonstrated that lysophosphatidic acid (LPA) enhances vascular endothelial growth factor-C (VEGF-C) expression, a lymphangiogenic factor, through activating it receptors LPA1/3 in prostate cancer (PCa) cells. Moreover, hyperglycemia up-regulates autotaxin (ATX) expression, a LPA-generating enzyme. Therefore, we propose that high glucose promotes VEGF-C expression through LPA signaling in PCa cells. Methods: Pharmacological inhibitors and siRNAs were utilized to investigate the molecular mechanism of high glucose-induced VEGF-C expression. Real-time PCR and Western blot were used to determine the mRNA and protein expressions, respectively. Cellular bioenergetics analysis was performed to determine the glycolysis levels. Results: We demonstrated that the expressions of VEGF-C, ATX, and calreticulin were increased upon high glucose treatments in PC-3 cells. Moreover, high glucose-induced VEGF-C expression was mediated through the LPA1/3, PLC, Akt, ROS and LEDGF-dependent pathways. Additionally, high glucose enhanced the aerobic glycolysis via LPA1/3. Conclusion: These results indicated that hyperglycemia leads to LPA synthesis, and subsequent promoting pathological consequence of PCa. These novel findings could potentially provide new strategies for PCa treatments. [ABSTRACT FROM AUTHOR]

Abstract Lysophosphatidic acid (LPA) is a bioactive lipid growth factor which is present in high levels in serum and platelets. LPA binds to its specific G-protein-coupled receptors, including LPA 1 to LPA 6 , thereby regulating various physiological functions, including cancer growth, angiogenesis, and lymphangiogenesis. Our previous study showed that LPA promotes the expression of the lymphangiogenic factor vascular endothelial growth factor (VEGF)-C in prostate cancer (PCa) cells. Interestingly, LPA has been shown to regulate the expression of calreticulin (CRT), a multifunctional chaperone protein, but the roles of CRT in PCa progression remain unclear. Here we investigated the involvement of CRT in LPA-mediated VEGF-C expression and lymphangiogenesis in PCa. Knockdown of CRT significantly reduced LPA-induced VEGF-C expression in PC-3 cells. Moreover, LPA promoted CRT expression through LPA receptors LPA 1 and LPA 3 , reactive oxygen species (ROS) production, and phosphorylation of eukaryotic translation initiation factor 2α (eIF2α). Tumor-xenografted mouse experiments further showed that CRT knockdown suppressed tumor growth and lymphangiogenesis. Notably, clinical evidence indicated that the LPA-producing enzyme autotaxin (ATX) is related to CRT and that CRT level is highly associated with lymphatic vessel density and VEGF-C expression. Interestingly, the pharmacological antagonist of LPA receptors significantly reduced the lymphatic vessel density in tumor and lymph node metastasis in tumor-bearing nude mice. Together, our results demonstrated that CRT is critical in PCa progression through the mediation of LPA-induced VEGF-C expression, implying that targeting the LPA signaling axis is a potential therapeutic strategy for PCa. Highlights • LPA regulates VEGF-C expression via calreticulin and subsequently induces lymphangiogenesis in prostate cancer cells. • LPA signaling is highly correlated with CRT, VEGF-C, and lymphatic vessel density in clinical prostate cancer patients. • Blockade of LPA signaling in prostate cancer cells significantly suppresses lymphangiogenesis and lymph node metastasis. [ABSTRACT FROM AUTHOR]

Highlights: [•] LPA-induced VEGF-A expression was regulated by HIF-1α and ARNT. [•] PI3K mediated LPA-induced VEGF-A expression. [•] AHR signaling inhibited LPA-induced VEGF-A expression in PC-3 cells. [ABSTRACT FROM AUTHOR]

Abstract: Photoluminescence (PL) spectra of a quaternary alloy In0.014Al0.105Ga0.881N thin film grown by low pressure metalorganic chemical vapor deposition (MOCVD) are studied experimentally in the temperature range of 10–300K. It is shown that the temperature dependence can be well studied by the Eliseev''s model to characterize the scale of the exciton-localization effects for the exciton localization energy. Moreover, the Urbach energy was determined from an analysis of the low-energy side of the PL lineshape. From the temperature dependence of Urbach energy, the value of Urbach energy can be described by the Einstein oscillator model which takes into consideration the contributions from both the thermal and structural disorders. [Copyright &y& Elsevier]

Abstract: The structural and optical properties of ZnO films deposited on Si substrate following rapid thermal annealing (RTA) have been investigated by X-ray diffraction (XRD), atomic force microscopy (AFM), and photoluminescence (PL) measurements. After RTA treatment, the XRD spectra have shown an effective relaxation of the residual compressive stress, an increase of the intensity and narrowing of the full-width at half-maximum (FWHM) of the (002) diffraction peak of the as-grown ZnO film. AFM images show roughening of the film surface due to increase of grain size after RTA. The PL spectrum reveals a significant improvement in the UV luminescence of ZnO films following RTA at 800°C for 1min. [Copyright &y& Elsevier]

Abstract: The influence of rapid thermal annealing (RTA) on the optical and structural properties of ZnO thin films grown on Si substrate has been investigated by X-ray diffraction (XRD), photoluminescence (PL), and Raman scattering (RS) measurements. The relaxation of the residual stress by increasing the annealing temperature during the RTA process was observed by the measured shift of (002) XRD diffraction peak towards 34.40∘ and the shift of RS (high) mode closer to 437 cm−1. The process also resulted in a reduction of the measured full-width at half maximum (FWHM) of the PL emission line and that of the asymmetrical broadening of RS (high) mode. The observed changes have demonstrated that RTA is a viable technique for improving the crystalline quality of ZnO/Si films. [Copyright &y& Elsevier]

The article reports on how the authors reached their clinical decision of whether cardiac rehabilitation improved the quality of life of a man with coronary artery disease who received percutaneous transluminal coronary angioplasty (PTCA) with the insertion of a stent. The authors, who are physical therapists, conducted literature searches through the MEDLINE medical electronic database and initially searched with the keywords cardiac rehabilitation, exercise training, and PTCA. The authors summarize the clinical trials that they read. Based on their findings through the literature search, the authors conclude that cardiac rehabilitation did improve patients' quality of life after PTCA.

Lysophosphatidic acid (LPA) is a bioactive lipid mediator primarily derived from membrane phospholipids. LPA initiates cellular effects upon binding to a family of G protein-coupled receptors, termed LPA receptors (LPAR1 to LPAR6). LPA signaling drives cell migration and proliferation, cytokine production, thrombosis, fibrosis, angiogenesis, and lymphangiogenesis. Since the expression and function of LPA receptors are critical for cellular effects, selective antagonists may represent a potential treatment for a broad range of illnesses, such as cardiovascular diseases, idiopathic pulmonary fibrosis, voiding dysfunctions, and various types of cancers. More new LPA receptor antagonists have shown their therapeutic potentials, although most are still in the preclinical trial stage. This review provided integrative information and summarized preclinical findings and recent clinical trials of different LPA receptor antagonists in cancer progression and resistance. Targeting LPA receptors can have potential applications in clinical patients with various diseases, including cancer. [ABSTRACT FROM AUTHOR]

Temperature-dependent photoluminescence (PL) and time-resolved photoluminescence (TRPL) are measured for the (Ga1-xZnx)(N1-xOx) solid solution with x = 0.22 to study its luminescence properties. PL result shows that the material exhibits visible luminescence at around 1.87 eV (663 nm) with a broad emission band even at room temperature. The origin of luminescence mechanism can be attributed to the radiative recombination of the electrons bound to donors and the holes bound to acceptors. The investigation from the integrated PL intensity and TRPL as a function of temperature indicates that the activation energy for thermalizing the electrons bound to a donor dominates the luminescence behavior in the (Ga1-xZnx)(N1-xOx) solid solution. [ABSTRACT FROM AUTHOR]

Prostate cancer (PCa) is the most common noncutaneous cancer in men worldwide. One of its major treatments is androgen deprivation therapy, but PCa frequently relapses as aggressive castration resistant local tumors and distal metastases. Hence, the development of novel agents or treatment modalities for advanced PCa is crucial. Many tumors, including PCa, first metastasize to regional lymph nodes via lymphatic vessels. Recent findings demonstrate that the bioactive lipid lysophosphatidic acid (LPA) promotes PCa progression by regulating vascular endothelial growth factor-C (VEGF-C), a critical mediator of tumor lymphangiogenesis and lymphatic metastasis. Many of the underlying molecular mechanisms of the LPA–VEGF-C axis have been described, revealing potential biomarkers and therapeutic targets that may aid in the diagnosis and treatment of advanced PCa. Herein, we review the literature that illustrates a functional role for LPA signaling in PCa progression. These discoveries may be especially applicable to anti-lymphangiogenic strategies for the prevention and therapy of metastatic PCa. [ABSTRACT FROM AUTHOR]

Atherosclerosis is characterized by the plaque formation that restricts intraarterial blood flow. The disturbed blood flow with the associated oscillatory stress (OS) at the arterial curvatures and branch points can trigger endothelial activation and is one of the risk factors of atherosclerosis. Many studies reported the mechanotransduction related to OS and atherogenesis; however, the transcriptional and posttranscriptional regulatory mechanisms of atherosclerosis remain unclear. Herein, we investigated the role of N6-methyladenosine (m6A) RNA methylation in mechanotransduction in endothelial cells (ECs) because of its important role in epitranscriptome regulation. We have identified m6A methyltransferase METTL3 as a responsive hub to hemodynamic forces and atherogenic stimuli in ECs. OS led to an up-regulation of METTL3 expression, accompanied by m6A RNA hypermethylation, increased NF-κB p65 Ser536 phosphorylation, and enhanced monocyte adhesion. Knockdown of METTL3 abrogated this OS-induced m6A RNA hypermethylation and other manifestations, whileMETTL3 overexpression led to changes resembling the OS effects. RNA-sequencing and m6A-enhanced crosslinking and immunoprecipitation (eCLIP) experiments revealed NLRP1 and KLF4 as two hemodynamics-related downstream targets of METTL3-mediated hypermethylation. The METTL3-mediated RNA hypermethylation up-regulated NLRP1 transcript and downregulated KLF4 transcript through YTHDF1 and YTHDF2 m6A reader proteins, respectively. In the in vivo atherosclerosis model, partial ligation of the carotid artery led to plaque formation and upregulation of METTL3 and NLRP1, with down-regulation of KLF4; knockdown of METTL3 via repetitive shRNA administration prevented the atherogenic process, NLRP3 up-regulation, and KLF4 down-regulation. Collectively, we have demonstrated thatMETTL3 serves a central role in the atherogenesis induced by OS and disturbed blood flow. [ABSTRACT FROM AUTHOR]

Background: The painDETECT questionnaire (PDQ) is a useful tool for screening of patients with neuropathic pain. This study aimed to translate the PDQ into the Malay language (PDQ-M) and to achieve cross-cultural adaptation of the questionnaire for use in Malaysia. Methods: The translation and cultural adaptation process of the English version of PDQ was performed based on international guidelines. Subsequently, 97 patients with neuropathic and nociceptive pain based on clinician's diagnoses were recruited to complete three-type numeric rating scale (NRS) of pain followed by PDQ-M. Results: On the basis of cognitive debriefing, several changes of the translated PDQ-M were made. A total of 53 patients with neuropathic pain and 44 with nociceptive pain (54.6% females, 45.4% males, mean age 52.4 years ± 14.2) were recruited into this study. The most common class of analgesia prescribed for patients with neuropathic pain was anti-convulsant, whereas co-analgesic therapy, which includes NSAID and COX-2 inhibitor, was the most prescribed for patients with nociceptive pain. Combination analgesia was used in 32.1% of those with neuropathic pain, and 11.4% of patients with nociceptive pain. The median time taken for respondents to complete the questionnaire was 420 seconds. In regression analysis, active smoking (beta 0.586, p<0.001) and female gender (beta -0.422, p=0.008) were associated with higher PDQ-M scores only among those with neuropathic pain. Conclusions: The Malay version of the painDETECT questionnaire was translated and cross-culturally adapted for ease of understanding among the local population via careful face-to-face interview. [ABSTRACT FROM AUTHOR]

We report the characteristics of reflectance spectra of the 15- and 20-period ZnTe/ZnSe distributed Bragg reflector grown on GaAs (001) substrates by molecular beam epitaxy. The reflectance spectra measured at various incident angles and polarizations were investigated by the theoretical curves simulated using transfer matrix method. The wavelength variation of the refractive indices described by Sellmeier equation and random thickness model were also considered for the interpretation of the experimentally observed curves. An omnidirectional reflection range defined from the edge of incident-angle-dependent reflection band with TE and TM polarizations is about 15 nm, and is consistent with the observed experimental curves. The results showed that the selected ZnTe and ZnSe materials are suitable for constructing multilayer structures having omnidirectional reflection band. [ABSTRACT FROM AUTHOR]

Highlights: [•] LPA induces ROS generation through LPA1 and LPA3. [•] LPA induces ROS generation by activating PLC. [•] PKCζ mediates LPA-induced ROS generation. [ABSTRACT FROM AUTHOR]

Abstract  To form a low noise figure and uniform shortpass band in optical fiber communications an improved automatic filtered power control (AFPC) pumping method is proposed here. A modulated single laser signal was entered in a closed feedback loop, in which the erbium-doped fiber amplifier (EDFA) was used as a part of the AFPC loop. Owing to the constant filtered signal and the quadrature phase shift delay inside the feedback loop, an optical pass band was uniformly formed. This EDFA attains high performance with a low noise figure simultaneously. The method was successfully applied to the fabrication of practical 12.0 m length of erbium-doped fiber pumped at 980 nm wavelength and 20 dBm power. Experiments prove that the signal gain of the loop remain flat in the range of 18.2 to 22.4 dB with a worst case error of ±0.5 dB and the noise figure was reduced by 2.2 dB at optimal, which correspond to a shortpass range of 40 nm band pass from 1525 nm to 1565 nm in wavelength. Of course, it should be possible to extent the system performance to all pumping configurations for semiconductor optical amplifiers. This provides the simplest and most economical way to transmit a well-defined band of modulated laser signal and to reject all other unwanted radiation. [ABSTRACT FROM AUTHOR]

We previously showed that chronic insulin infusion induces insulin resistance, hyperendothelinemia, and hypertension in rats (C. C. Juan, V. S. Fang, C. F. Kwok, J. C. Perng, Y. C. Chou, and L. T. Ho. Metabolism 48: 465-471, 1999). Endothelin-1 (ET-l), a potent vasoconstrictor, is suggested to play an important role in maintaining vascular tone and regulating blood pressure, and insulin increases ET-1 production in vivo and in vitro. In the present study, BQ-610, a selective endothelin A receptor antagonist, was used to examine the role of ET-1 in insulin-induced hypertension in rats. BQ-610 (0.7 mg/ml; 0.5 ml/kg body wt) or normal saline was given intraperitoneally two times daily for 25 days to groups of rats infused with either saline or insulin (2 U/day via sc-implanted osmotic pumps), and changes in plasma levels of insulin, glucose, and ET-1 and the systolic blood pressure were measured over the experimental period, whereas changes in insulin sensitivity were examined at the end of the experimental period. Plasma insulin and ET-1 levels were measured by RIA, plasma glucose levels using a glucose analyzer, systolic blood pressure by the tail-cuff method, and insulin sensitivity by an oral glucose tolerance test. Our studies showed that insulin infusion caused sustained hyperinsulinemia in both saline- and BQ-610-injected rats over the infusion period. After pump implantation (2 wk), the systolic blood pressure was significantly higher in insulin-infused rats than in saline-infused rats in the saline-injected group (133 ± 3.1 vs. 113 ± 1.1 mmHg, P < 0.05) but not in the BQ-610-injected group (117 ± 1.2 vs. 117 ± 1.8 mmHg). Plasma ET-1 levels in both sets of insulin-infused rats were higher than in saline-infused controls (2.5 ± 0.6 and 2.5 ± 0.8 vs. 1.8 ± 0.4 and 1.7 ± 0.3 pmol/l, P < 0.05). Oral glucose tolerance tests showed that BQ-610 treatment did not prevent the insulin resistance caused by chronic insulin infusion. No significant changes were found in insulin sensitivity and blood pressure in saline-infused rats treated with BQ-610. In a separate experiment, insulin infusion induced the increase in arterial ET-1 content, hypertension, and subsequent plasma ET-1 elevation in rats. These results suggest that, in the insulin infusion rat model, ET-1 plays a mediating role in the development of hypertension, but not of insulin resistance. [ABSTRACT FROM AUTHOR]

Communication between cells and extracellular environments is of interest because of its critical roles in cell development and differentiation. Particularly, this signal transduction is commonly believed to rely on the contact and binding of the participating molecules/proteins, suggesting that the binding distance needed is less than a few nanometers. However, it is difficult to precisely match the rapidly binding interaction which depends on the probability of molecular collision in living systems, raising a hypothesis that another mechanism exists, could promote this signal communication, and remains unknown. Here we report that a long-range signal delivery over 10-μm and 20-μm polydimethylsiloxane (PDMS) barriers can be observed in microfluidically tetracycline (Tet) inducible expression systems. Results show that a significant increment of the long-range induced green fluorescent protein in human embryonic kidney 293T (HEK 293T) cells by the stimulation of Tet is demonstrated, and that such a signal induction is not dominated by Tet diffusion and displays a specific bindingless property. In addition, our experimental results, combined with theoretical modeling, suggest that this communication exhibits a bump-shaped characteristic depending on barrier thickness, materially structural property, surface roughness, and agonist concentration. It strongly relies on the PDMS barrier to delivery signal; therefore, we call such a mechanism as "wired" cell communication instead of wireless. These results could ignite interests in the novel and "wired" cell communication, which we call it X-signal, and in the use of such systems for the study of cellular biology and development of new drug. [ABSTRACT FROM AUTHOR]

The cellular signal transduction is commonly believed to rely on the direct "contact" or "binding" of the participating molecule reaction that depends positively on the corresponding molecule concentrations. In living systems, however, it is somewhat difficult to precisely match the corresponding rapid "binding," depending on the probability of molecular collision, existing in the cellular receptor-ligand interactions. Thus, a question arises that if there is another mechanism (i.e., bindingless) that could promote this signal communication. According to this hypothesis, we report a cellular model based on the examination of intracellular calcium concentration to explore whether the unidentified signal delivery in cells exists, via a microfluidic device. This device was designed to isolate the cells from directly contacting with the corresponding ligands/molecules by the particular polydimethylsiloxane (PDMS) membranes with different thicknesses. Results show a significant increment of calcium mobilization in human prostate cancer PC-3 cells by the stimulation of endothelin-1, even up to a separated distance of 95 μm. In addition, these stimulated signals exhibited a bump-shaped characteristics depending on the membrane thickness. When the PDMS membrane is capped by SiO2, a particular trait that resembles the ballistic signal conduction was observed. A theoretical model was developed to describe the signal transport process across the PDMS membrane. Taken together, these results indicate that the unidentified signal (ligand structural information) delivery could occur in cells and be examined by the proposed approach, exhibiting a bindingless communication manner. Moreover, this approach and our finding may offer new opportunities to establish a robust and cost-effective platform for the study of cellular biology and new drug development. [ABSTRACT FROM AUTHOR]

The effect of carrier localization in InGaN/GaN multiple quantum wells (MQWs) light-emitting diodes is investigated by photoluminescence (PL) and time-resolved PL (TRPL) measurements. PL results show that two peaks obtained by Gaussian fitting both relate to the emission from localized states. By fitting the TRPL lifetimes at various emission energies, two localization depths corresponding to the In-rich regions and quasi-MQWs regions are obtained. Using a model we proposed, we suggest that compositional fluctuations of In content and variation of well width are responsible for carrier localization in In-rich regions and quasi-MQWs regions, respectively. [ABSTRACT FROM AUTHOR]

Hutchinson–Gilford progeria syndrome (HGPS) is a rare laminopathy that produces a mutant form of prelamin A, known as Progerin, resulting in premature aging. HGPS cells show morphological abnormalities of the nuclear membrane, reduced cell proliferation rates, accumulation of reactive oxygen species (ROS), and expression of senescence markers. Lysophosphatidic acid (LPA) is a growth factor‐like lipid mediator that regulates various physiological functions via activating multiple LPA G protein‐coupled receptors. Here, we study the roles of LPA and LPA receptors in premature aging. We report that the protein level of LPA3 was highly downregulated through internalization and the lysosomal degradation pathway in Progerin‐transfected HEK293 cells. By treating Progerin HEK293 cells with an LPA3 agonist (OMPT, 1‐Oleoyl‐2‐O‐methyl‐rac‐glycerophosphothionate) and performing shRNA knockdown of the Lpa3r transcript in these cells, we showed that LPA3 activation increased expression levels of antioxidant enzymes, consequently inhibiting ROS accumulation and ameliorating cell senescence. LPA3 was shown to be downregulated in HGPS patient fibroblasts through the lysosomal pathway, and it was shown to be crucial for ameliorating ROS accumulation and cell senescence in fibroblasts. Moreover, in a zebrafish model, LPA3 deficiency was sufficient to cause premature aging phenotypes in multiple organs, as well as a shorter lifespan. Taken together, these findings identify the decline of LPA3 as a key contributor to the premature aging phenotypes of HGPS cells and zebrafish. [ABSTRACT FROM AUTHOR]

Three dual-wavelength InGaN/GaN multiple quantum well (MQW) light emitting diodes (LEDs) with increasing indium content are grown by metal-organic chemical vapor deposition, which contain six periods of low-In-content MQWs and two periods of high-In-content MQWs. For the low-In-content MQWs of three studied samples, their internal quantum efficiency (IQE) shows a rising trend as the emission wavelength increases from 406 nm to 430 nm due to the suppression of carriers escape from the wells to the barriers. However, for the high-In-content MQWs, the sample IQE falls rapidly with a further increase of emission wavelength from 496 nm to 575 nm. Theoretical calculation reveals that the electron-hole wave function overlap in the high-In-content MQWs is reduced because of an increase in the internal polarization field as indium content is increased. In addition, time-resolved photoluminescence decay curves show that the carriers generated in the low-In-content MQWs can be effectively transferred to the high-In-content part through the reabsorption process. However, the transfer time gradually becomes longer as emission wavelength increases, which means a reduction of carrier transfer rate between the different indium content MQWs. Furthermore, nonradiative recombination is enhanced in the high-In-content MQWs with longer emission wavelength due to the decline of crystal quality. Therefore, the fast drop of IQE for high-In-content MQWs can be attributed to the increase of the internal polarization field, the decrease of carrier transfer efficiency, and the enhanced nonradiative recombination. This research has a certain guiding value for an understanding of the recombination mechanism in the InGaN/GaN MQWs and for achieving high quality multiple-wavelength LEDs with better performance. [ABSTRACT FROM AUTHOR]

We have investigated optical characteristics and carrier recombination dynamics of { 1 1 ¯ 01 } and { 11 2 ¯ 2 } semipolar InGaN/GaN quantum wells of light-emitting diodes (LEDs) structures grown by selective area epitaxy (SAE). The semipolar samples exhibit higher radiative recombination rates than the polar one at the same temperature. Self-consistent Poisson and 6 × 6 k·p Schrödinger calculation results exhibit the same trend. Moreover, we explained the weakened S-shaped temperature-dependent photoluminescence (PL) peak energy of semipolar samples by their weak phonon-assisted carrier in-plane hopping effect, which is further verified by PL spectra-dependent decay times and temperature-dependent radiative lifetimes. [ABSTRACT FROM AUTHOR]

We present the incident-angle-dependent reflectance spectra of the 10-period ZnO/MgO multilayer films deposited on Si by sputtering technique. As increasing the incident angle, the resonant wavelength and bandwidth of the measured reflectance spectra exhibit redshift and narrower, respectively. The theoretical curves using transfer matrix method taken account of transverse electric (TE) and transverse magnetic (TM) polarizations are calculated to well describe the variations in the behavior of the experimental spectra. The simulated TE- and TM-reflection band at different angles can evaluate the bandwidth of the resonance band and provide valuable parameters to design an omnidirectional-reflection band in selected multilayer structure. [ABSTRACT FROM AUTHOR]

Abstract: Sphingosine 1-phosphate (S1P) is a bioactive lysophospholipid that binds to a family of G protein-coupled receptors (GPCRs), termed S1P1–S1P5. Our previous study has reported that S1P induces autophagy in human prostate cancer PC-3 cell. In addition, S1P-induced autophagy plays a prosurvival role in PC-3 cells. Accumulating evidence has shown that the autophagy responses triggered by ER stress signaling have cytoprotective effects. Thus, we attempted to investigate whether S1P-induced autophagy is a result of triggering ER stress in PC-3 cells. By monitoring XBP-1 mRNA splicing, a characteristic of ER stress, we demonstrate that S1P triggers ER stress in a concentration-dependent and time-dependent manner. Moreover, DiH S1P, a membrane-nonpermeable S1P analog without intracellular effects also enhances ER stress. Meanwhile, we also show that S1P5 is required for S1P-induced ER stress by using RNA interference experiments. Furthermore, signaling analyses revealed that PI3K, PLC, and ROS production were involved in S1P's effects on ER stress induction. On the other hand, knockdown of XBP-1 abolished S1P-induced autophagy. In summary, our results demonstrate for the first time that the extracellular S1P-triggered ER stress is responsible for autophagy induction in PC-3 cells. [Copyright &y& Elsevier]

Dioxins are byproducts from incomplete combustion processes and belong to a group of mostly toxic chemicals known as persistent organic pollutants, and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is considered to be the most toxic species of all dioxin-like compounds. Analytical chemical processes are employed to determine the specific dioxin content in environmental samples. However, cost-ineffectiveness and excess time consumption limit their routine utilization. The aryl hydrocarbon receptor (AhR) is the major TCDD receptor. Upon binding to dioxin, the AhR dissociates from Hsp90 and other cofactors. TCDD-bound AhR subsequently translocates to the nucleus and interacts with the AhR nuclear translocator (Arnt) to induce signal transduction. Here, we describe a highly sensitive and cost-effective alternative assay based on detecting stability of bioluminescence signals. We generated cells that stably co-express Renilla luciferase tagged-AhR (AhR-RL), Ah receptor-interacting protein (AIP), p23 and yellow fluorescent protein-tagged Arnt (Arnt-YFP) (AAPA cells) for detection of dioxin-like compounds. Treatment with 3-methylcholanthrene (3MC), AhR agonist, enhanced the interaction between AhR and Arnt and avoided proteosomal degradation. In addition, treatment with 3MC or TCDD stabilized Renilla luminescence from AhR-RL of AAPA cell-free extracts in a concentration-dependent manner. The TCDD detection limit in this cell-free system was as low as 10−18 M. These results highlight the potential of AAPAA cell-free extracts to detect dioxin-like pollutants. [ABSTRACT FROM AUTHOR]

Two ultraviolet InGaN/GaN light emitting diodes (LEDs) with and without InGaN underlying layer beneath the multiple quantum wells (MQWs) were grown by metal-organic vapor phase epitaxy. Based on the photoluminescence excitation measurements, it was found that the Stokes shift of the sample with a 10-nm-thick InGaN underlying layer was about 64 meV, which was smaller than that of the reference sample without InGaN underlying layer, indicating a reduced quantum-confined Stark effect (QCSE) due to the decrease of the piezoelectric polarization field in the MQWs. In addition, by fitting the photon energy dependence of carrier lifetime values, the radiative recombination lifetime of the sample with and without InGaN underlying layer were obtained about 1.22 and 1.58 ns at 10 K, respectively. The shorter carrier lifetime also confirmed that the QCSE in the MQWs was weakened after inserting the InGaN underlying layer. In addition, although the depth of carrier localization in the sample with InGaN underlying layer became smaller, the nonradiative recombination centers (NRCs) inside it decreased, and thus suppressed the nonradiative recombination process significantly according to the electroluminescence measurement results. Compared to the reference sample, the efficiency droop behavior was delayed in the sample with InGaN underlying layer and the droop effect was also effectively alleviated. Therefore, the enhanced light-emission efficiency of ultraviolet InGaN/GaN MQW LEDs could be attributed to the decrease of QCSE and NRCs. [ABSTRACT FROM AUTHOR]

Clinical evidence suggests that lymphangiogenesis and lymphatic metastasis are important processes during the progression of prostate cancer. Vascular endothelial growth factor (VEGF)-C was shown to be a key regulator in these processes. Our previous studies demonstrated that lysophosphatidic acid (LPA), a low-molecular-weight lipid growth factor, enhances VEGF-C expression in human endothelial cells. We previously demonstrated that the LPA receptor plays an important role in lymphatic development in zebrafish embryos. However, the effects of LPA on VEGF-C expression in prostate cancer are not known. Herein, we demonstrate that LPA up-regulated VEGF-C expression in three different human prostate cancer cell lines. In PC-3 human prostate cancer cells, the enhancing effects of LPA were mediated through both LPA1 and LPA3. In addition, reactive oxygen species (ROS) production and lens epithelium-derived growth factor (LEDGF) expression were involved in LPA1/3-dependent VEGF-C expression. Furthermore, autotaxin (ATX), an enzyme responsible for LPA synthesis, also participates in regulating VEGF-C expression. By interrupting LPA1/3 of PC-3, conditioned medium (CM) - induced human umbilical vein endothelial cell (HUVEC) lymphatic markers expression was also blocked. In summary, we found that LPA enhances VEGF-C expression through activating LPA1/3-, ROS-, and LEDGF-dependent pathways. These novel findings could potentially shed light on developing new strategies for preventing lymphatic metastasis of prostate cancer. [ABSTRACT FROM AUTHOR]

The only curative treatment for hepatic failure is liver transplantation. Unfortunately, this treatment has several major limitations, as for example donor organ shortage. A previous report demonstrated that transplantation of induced pluripotent stem cells without reprogramming factor c-Myc (3-genes iPSCs) attenuates thioacetamide- induced hepatic failure with minimal incidence of tumorigenicity. In this study, we investigated whether 3-genes iPSC transplantation is capable of rescuing carbon tetrachloride (CCl4)-induced fulminant hepatic failure and hepatic encephalopathy in mice. Firstly, we demonstrated that 3-genes iPSCs possess the capacity to differentiate into hepatocyte-like cells (iPSC-Heps) that exhibit biological functions and express various hepatic specific markers. 3-genes iPSCs also exhibited several antioxidant enzymes that prevented CCl4-induced reactive oxygen species production and cell death. Intraperitoneal transplantation of either 3-genes iPSCs or 3-genes iPSC-Heps significantly reduced hepatic necrotic areas, improved hepatic functions, and survival rate in CCl4-treated mice. CCl4-induced hepatic encephalopathy was also improved by 3-genes iPSC transplantation. Hoechst staining confirmed the successful engraftment of both 3-genes iPSCs and 3-genes iPSC-Heps, indicating the homing properties of these cells. The most pronounced hepatoprotective effect of iPSCs appeared to originate from the highest antioxidant activity of 3-gene iPSCs among all transplanted cells. In summary, our findings demonstrated that 3-genes iPSCs serve as an available cell source for the treatment of an experimental model of acute liver diseases. [ABSTRACT FROM AUTHOR]

Although surgery or the combination of chemotherapy and radiation are reported to improve the quality of life and reduce symptoms in patients with oral cancer, the prognosis of oral cancer remains generally poor. DNA alkylating agents, such as N-mustard, play an important role in cancer drug development. BO-1051 is a new 9-anilinoacridine N-mustard-derivative anti-cancer drug that can effectively target a variety of cancer cell lines and inhibit tumorigenesis in vivo. However, the underlying mechanism of BO-1051-mediated tumor suppression remains undetermined. In the present study, BO-1051 suppressed cell viability with a low IC50 in oral cancer cells, but not in normal gingival fibroblasts. Cell cycle analysis revealed that the tumor suppression by BO-1051 was accompanied by cell cycle arrest and downregulation of stemness genes. The enhanced conversion of LC3-I to LC3-II and the formation of acidic vesicular organelles indicated that BO-1501 induced autophagy. The expression of checkpoint kinases was upregulated as demonstrated with Western blot analysis, showing that BO-1051 could induce DNA damage and participate in DNA repair mechanisms. Furthermore, BO-1051 treatment alone exhibited a moderate tumor suppressive effect against xenograft tumor growth in immunocompromised mice. Importantly, the combination of BO-1051 and radiation led to a potent inhibition on xenograft tumorigenesis. Collectively, our findings demonstrated that BO-1051 exhibited a cytotoxic effect via cell cycle arrest and the induction of autophagy. Thus, the combination of BO-1051 and radiotherapy may be a feasible therapeutic strategy against oral cancer in the future. [ABSTRACT FROM AUTHOR]

Induced pluripotent stem cells formed by the introduction of only three factors, Oct4/Sox2/Klf4 (3-gene iPSCs), may provide a safer option for stem cell-based therapy than iPSCs conventionally introduced with four-gene iPSCs. Peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) plays an important role during brown fat development. However, the potential roles of PGC-1α in regulating mitochondrial biogenesis and the differentiation of iPSCs are still unclear. Here, we investigated the effects of adenovirus-mediated PGC-1α overexpression in 3-gene iPSCs. PGC-1α overexpression resulted in increased mitochondrial mass, reactive oxygen species production, and oxygen consumption. Microarray-based bioinformatics showed that the gene expression pattern of PGC-1α-overexpressing 3-gene iPSCs resembled the expression pattern observed in adipocytes. Furthermore, PGC-1α overexpression enhanced adipogenic differentiation and the expression of several brown fat markers, including uncoupling protein-1, cytochrome C, and nuclear respiratory factor-1, whereas it inhibited the expression of the white fat marker uncoupling protein-2. Furthermore, PGC-1α overexpression significantly suppressed osteogenic differentiation. These data demonstrate that PGC-1α directs the differentiation of 3-gene iPSCs into adipocyte-like cells with features of brown fat cells. This may provide a therapeutic strategy for the treatment of mitochondrial disorders and obesity. [ABSTRACT FROM AUTHOR]

Hematopoiesis, the complex developmental process that forms blood components and replenishes the blood system, involves multiple intracellular and extracellular mechanisms. We previously demonstrated that lysophosphatidic acid (LPA), a lipid growth factor, has opposing regulatory effects on erythrocyte differentiation through activation of LPA receptors 2 and 3; yet the mechanisms underlying this process remain unclear. In this study, LPA 2 is observed that highly expressed in common myeloid progenitors (CMP) in murine myeloid cells, whereas the expression of LPA 3 displaces in megakaryocyte-erythroid progenitors (MEP) of later stage of myeloid differentiation. Therefore, we hypothesized that the switching expression of LPA 2 and LPA 3 determine the hematic homeostasis of mammalian megakaryocytic-erythroid lineage. In vitro colony-forming unit assays of murine progenitors reveal that LPA 2 agonist GRI reduces the erythroblast differentiation potential of CMP. In contrast, LPA 3 agonist OMPT increases the production of erythrocytes from megakaryocyte-erythrocyte progenitor cells (MEP). In addition, treatment with GRI reduces the erythroid, CMP, and MEP populations in mice, indicating that LPA 2 predominantly inhibits myeloid differentiation at an early stage. In contrast, activation of LPA 3 increases the production of terminally differentiated erythroid cells through activation of erythropoietic transcriptional factor. We also demonstrate that the LPA 3 signaling is essential for restoration of phenylhydrazine (PHZ)-induced acute hemolytic anemia in mice and correlates to erythropoiesis impairment of Hutchinson-Gilford progeria Symptom (HGPS) premature aging expressed K562 model. Our results reveal the distinct roles of LPA 2 and LPA 3 at different stages of hematopoiesis in vivo , providing potentiated therapeutic strategies of anemia treatment. • The switching expression of LPA 2 and LPA 3 determine the homeostasis of mammalian megakaryocytic-erythroid lineage. • LPA 2 predominantly blocks myeloid lineage with impaired proliferation and increased apoptosis at the early stage. • LPA 3 signaling is an essential mediator of erythropoiesis at the latter stage and participate in aging-related anemia. • Activation of LPA 3 by agonist provides potentiated therapeutic strategies of anemia treatment. [ABSTRACT FROM AUTHOR]