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Pectobacterium carotovorum subsp. carotovorum (Pcc) is a Gram-negative phytopathogenic bacterium that produces carocin, a low-molecular-weight bacteriocin that can kill related strains in response to factors in the environment such as UV exposure or nutritional deficiency. The function of the catabolite activator protein (CAP), also known as the cyclic AMP receptor protein (CRP), as a regulator of carocin synthesis was examined. The crp gene was knocked out as part of the investigation, and the outcomes were assessed both in vivo and in vitro. Analysis of the DNA sequence upstream of the translation initiation site of carocin S3 revealed two putative binding sites for CRP that were confirmed using a biotinylated probe pull-down experiment. This study revealed that the deletion of crp inhibited genes involved in extracellular bacteriocin export via the flagellar type III secretion system and impacted the production of many low-molecular-weight bacteriocins. The biotinylated probe pull-down test demonstrated that when UV induction was missing, CRP preferentially attached to one of the two CAP sites while binding to both when UV induction was present. In conclusion, our research aimed to simulate the signal transduction system that controls the expression of the carocin gene in response to UV induction.

Cancer-related fatigue is the most common and longest-lasting symptom of discomfort experienced by cancer patients. Its effects on patients include physical, psychological, emotional, and cognitive stress, which greatly reduce quality of life. The field of mind-body integrated medicine has improved gradually in recent years, with many evidence-based studies supporting the efficacy of mindfulness as a symptom management strategy for cancer-related fatigue. Based on a review of the literature, this paper introduces the definition of cancer-related fatigue and related assessments and treatments, describes the origin of mindfulness and related concepts, and introduces mindfulness-based empirical treatment strategies for cancer-related fatigue, including mindfulness-based stress reduction and mindfulness-based cognitive therapy, and their effects. The findings are intended to provide clinicians with a reference for the future care of patients with cancer-related fatigue.與癌共處—正念於癌因性疲憊之臨床應用.癌因性疲憊為癌症病人最常經歷且為時最久的不適症狀，影響病人產生諸多層面上的困擾，如身體、心理、情緒及認知等，大幅降低其生活品質。近年來身心整合醫學（mind-body integrative medicine）開始發展，實證研究陸續顯示，正念（mindfulness）可作為癌因性疲憊之症狀管理策略。因此本文透過文獻回顧，簡介癌因性疲憊的定義、評估及處置，並歸納整理正念的源起與相關概念，介紹正念運用於癌因性疲憊之相關實證處理策略與成效，如正念減壓（mindfulness-based stress reduction）及正念認知療法（mindfulness-based cognitive therapy）等，藉此提供臨床工作者未來照護癌因性疲憊病人之參考。.

Constant DNA damage occurs in cells, and the cells are programmed to respond constitutively. This study explored the roles of ataxia-telangiectasia mutated interactor (ATMIN), one of the impaired pathways involving the DNA damage response (DDR) in mismatch repair-deficient [microsatellite instability (MSI)-high] colorectal carcinoma (CRC). Expression of ATMIN messenger RNA (mRNA) was detected in CRC specimens with microsatellite instability (MSI) characteristics. The effects of ectopic ATMIN expression and ATMIN knockdown on invasion abilities were evaluated in MSI-high cell lines, and liver metastasis ability was investigated in vivo. Protein-protein interactions were assessed by coimmunoprecipitation analyses in vitro. Decreased ATMIN expression was positively correlated with advanced stage of disease (P < 0.05), lymph node metastases (P < 0.05), and deeper invasion (P < 0.05) in MSI-high tumors. Transient or stable ATMIN knockdown significantly increased cell motility. Moreover, in the high-throughput microarray and gene set enrichment analysis, ATMIN was shown to act on the Wnt-signaling pathway via PARP1. This cascade influences β-catenin/transcription factor 4 (TCF4) binding affinity in MSI-high tumors, and PARP1 inhibition significantly decreased the number of metastases from ATMIN knockdown cancer cells. The results not only indicated the critical role of ATMIN, but also shed new light on PARP1 inhibitors, providing a basis for further clinical trials of MSI-high CRC.

Genomic instability is a key cancer indicator. It results from defects in the DNA damage response (DDR) and increased replication stress. Herein, we examined how ataxia-telangiectasia mutated interactor (ATMIN), a DDR pathway involved in mismatch repair-proficient (microsatellite stability [MSS]), acts in colorectal carcinoma (CRC). Firstly, ATMIN mRNA expression was detected in CRC specimens with MSS characteristics, and the effects of ectopic ATMIN expression and ATMIN knockdown on invasion abilities were gauged in MSS cell lines. To understand the molecular mechanism, co-immunoprecipitation analyses in vitro were employed. Interestingly, ATMIN expression was positively correlated with advanced stages (P < .001), lymph node metastases (P = .002), and deeper invasion (P = .037) in MSS tumors; and significantly changed the cell motility in vitro. In the high-throughput analysis, ATMIN was found to act on the Wnt signaling pathway via PARP1. PAPR1 inhibition, in turn, significantly decreased invasion abilities resulting from ATMIN overexpression in cancer cell. Taken together, ATMIN, which alters the Wnt signaling pathway regulating CRC progression, plays as a crucial prognostic factor in MSS tumors.

We develop a variational Bayesian (VB) approach for estimating large-scale dynamic network models in the network autoregression framework. The VB approach allows for the automatic identification of the dynamic structure of such a model and obtains a direct approximation of the posterior density. Compared to Markov Chain Monte Carlo (MCMC) based sampling approaches, the VB approach achieves enhanced computational efficiency without sacrificing estimation accuracy. In the simulation study conducted here, the proposed VB approach detects various types of proper active structures for dynamic network models. Compared to the alternative approach, the proposed method achieves similar or better accuracy, and its computational time is halved. In a real data analysis scenario of day-ahead natural gas flow prediction in the German gas transmission network with 51 nodes between October 2013 and September 2015, the VB approach delivers promising forecasting accuracy along with clearly detected structures in terms of dynamic dependence., Comment: 40 pages, 38 figures

Background: The management of hypertension remains suboptimal throughout the world. Methods: We performed a random-effects model meta-analysis of randomized controlled trials to determine the effectiveness and safety of sacubitril/valsartan (LCZ696) for the treatment of high arterial pressure. Relevant published articles from PubMed, Cochrane base, and Medline were examined, and the last search date was December 2020. Only published randomized controlled trials and double-blind studies were selected for further analysis. The mean reductions in systolic blood pressure (msSBP) and diastolic blood pressure (msDBP) in the sitting position, as well as the mean reductions in ambulatory systolic blood pressure (maSBP) and ambulatory diastolic blood pressure (maDBP), were assumed as efficacy endpoints. Adverse events (AEs) were considered as safety outcomes. Results: Ten studies with a total of 5931patients were included for analysis. Compared with placebo, LCZ696 had a significant reduction in msSBP (weight mean difference (WMD) = −6.52 mmHg, 95% confidence interval (CI): −8.57 to −4.47; p < 0.001), msDBP (WMD = −3.32 mmHg, 95% CI: −4.57 to −2.07; p < 0.001), maSBP (WMD = −7.08 mmHg, 95% CI: −10.48 to −3.68; p < 0.001), maDBP (WMD = −3.57 mmHg, 95% CI: −5.71 to −1.44, p < 0.001). In subgroup analysis, only 200 mg and 400 mg LCZ696 showed a significant BP reduction. There was no difference in the AE rate between the LCZ696 and placebo groups (WMD = 1.02, 95% CI: 0.83 to 1.27, p = 0.54). Egger’s test revealed a potential publication bias for msSBP (p = 0.025), but no publication bias for other outcomes. Conclusion: LCZ696 may reduce blood pressure more efficaciously than traditional therapy in hypertensive patients without increasing adverse effects.

Background Glycolysis machinery regulates cancer cell behavior. However, the roles of these glycolysis enzymes in oral squamous cell carcinoma (OSCC) progression remain unknown. Methods Fructose-bisphosphate aldolase C (ALDOC) expression in OSCC patients and cell lines was detected using quantitative real-time polymerase chain reaction (PCR). The functions of ALDOC in migration and invasion were determined using gain and loss of function approaches. An orthotopic OSCC animal model was performed to investigate the effects of ALDOC on metastasis and tumorigenesis in vivo. Results ALDOC expression is negatively significantly correlated with clinical outcome and cell migration in vitro and in vivo. ALDOC blocks adenosine triphosphate generation and lactate production, and mutation constructs of Arg42 and Lys146 functionally restore ALDOC-inhibited cell migration and invasion. Conclusion ALDOC functions as an OSCC prognosis marker clinically, and suppresses migration and invasion by its catalytic domain of Arg42 and Lys146. © 2015 Wiley Periodicals, Inc. Head Neck, 2015

Background/Purpose Deregulation of metabolic pathways is one of the hallmarks of cancer progression. Connective tissue growth factor (CTGF/CCN2) acts as a tumor suppressor in oral squamous cell carcinoma (OSCC). However, the role of CTGF in modulating cancer metabolism is still unclear. Methods OSCC cells stably overexpressing CTGF (SAS/CTGF) and shRNA against CTGF (TW2.6/shCTGF) were established. Oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) were examined by the Seahorse XF24 analyzer. The expression of CTGF and mitochondrial biogenesis related genes was measured by real-time polymerase chain reaction or Western blot analysis. Results CTGF decreased OCR, ECAR, adenosine triphosphate (ATP) generation, mitochondrial DNA (mtDNA), and mitochondrial transcription factor A (mtTFA) protein expression in OSCC cells. Overexpression of mtTFA restored CTGF-decreased OCR, ECAR, mtDNA copy number, migration and invasion of SAS/CTGF cells. Immunoprecipitation assay showed a higher level of ubiquitinated mtTFA protein after CTGF treatment. MG132, an inhibitor of proteasomal degradation, reversed the effect of CTGF on mtTFA protein expression in SAS cells. Conclusion CTGF can decrease glycolysis, mitochondrial oxidative phosphorylation, ATP generation, and mtDNA copy number by increasing mtTFA protein degradation through ubiquitin proteasome pathway and in turn reduces migration and invasion of OSCC cells. Therefore, CTGF may be developed as a potential additive therapeutic drug for oral cancer in the near future.

Abnormalities in the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway are commonly observed in human cancers and contribute to chemotherapy resistance. Combination therapy, involving the use of molecular targeted agents and traditional cytotoxic drugs, may represent a promising strategy to lower resistance and enhance cytotoxicity. Here, we demonstrate the efficacy of an Akt inhibitor, MK-2206, in increasing the cytotoxic effect of either paclitaxel (Taxol) or cisplatin against the ovarian cancer cell lines SKOV3 (with constitutively active Akt) and ES2 (with inactive Akt). Sequential treatment of Taxol or cisplatin, followed by MK-2206, induced a synergistic inhibition of cell proliferation and effectively promoted cell death, either by inhibiting the phosphorylation of Akt and its downstream effectors 4E-BP1 and p70S6K in SKOV3 cells or by restoring p53 levels, which were downregulated after Taxol or cisplatin treatment, in ES2 cells. Combination treatment also downregulated the pro-survival protein Bcl-2 in both SKOV3 and ES2 cells, which may have contributed to cell death. In addition, we discovered that Taxol/MK-2206 or cisplatin/MK-2206 combination treatment resulted in significant enhancement of intracellular reactive oxygen species (ROS) induced by MK-2206, in both SKOV3 and ES2 cells; however, MK-2206-induced growth inhibition was reversed by a ROS scavenger only in ES2 cells. MK-2206 also suppressed DNA repair, particularly in SKOV3 cells. Taken together, our results demonstrate that the Akt inhibitor MK-2206 enhances the efficacy of cytotoxic agents in both Akt-active and Akt-inactive ovarian cancer cells but through different mechanisms.

We demonstrate a successful selective growth of Si0.3Ge0.7 quantum dots (QDs) over array of p+-Si nanopillars using a low-pressure chemical vapor deposition technique, and hereafter realized high-performance QD broadband photodiodes for visible to near-infrared photodetection based on heterostructures of indium tin oxide/Si0.3Ge0.7 QD/Si pillar. Thanks to effective hole confinement and thus a built-in electric field within the SiGe QD, high ratios of photocurrent to dark current of ~2200, 100, and 30, respectively, were measured on our SiGe QDs-based photodiodes under illumination of 9 mW/cm2 at wavelength of 500-800, 1300, and 1500 nm. The QD photodiode exhibits a very low dark current density of 3.2 × 10-8 A/cm2 and a tunable power-dependent linearity by applied voltage through the competition of electron drift and carrier recombination processes.

We reported previously that a hemiasterlin derivative BF65 is a potent anticancer agent that can inhibit microtubule assembly. Here we show that a more potent stereospecific diastereomer (R)(S)(S)-BF65 can synergize with an allosteric Akt inhibitor MK-2206 to suppress the growth of SKOV3 ovarian cancer cells with constitutively active Akt. (R)(S)(S)-BF65 induced mitotic arrest and MK-2206 caused G0/G1 arrest, while the combination of both induced simultaneous G0/G1 and G2/M cell cycle arrest. (R)(S)(S)-BF65 induced phosphorylation and inactivation of Bcl-2, and downregulated Mcl-1, consequently may lead to apoptosis. (R)(S)(S)-BF65 inhibited mitogen-activated protein kinases (MAPKs), which may stimulate cell proliferation upon activation. (R)(S)(S)-BF65 also induced DNA damage after long-term treatment. MK-2206 is known to inhibit phosphorylation and activation of Akt and suppress cancer cell growth. The combination of (R)(S)(S)-BF65 and MK-2206 also inhibited the Akt pathway. Interestingly, MK-2206 upregulated Bcl-2 and induced activation of MAPKs in SKOV3 cells; however, when combined with (R)(S)(S)-BF65, these prosurvival effects were reversed. The combination also more significantly decreased Mcl-1 protein, increased PARP cleavage, and induced γ-H2AX, a DNA damage marker. Remarkably, MK-2206 enhanced the microtubule depolymerization effect of (R)(S)(S)-BF65. The combination of (R)(S)(S)-BF65 and MK-2206 also markedly inhibited cell migration. Thus, MK-2206 synergizes with (R)(S)(S)-BF65 to inhibit SKOV3 cell growth via downregulating the Akt signaling pathway, and enhancing the microtubule disruption effect of (R)(S)(S)-BF65. (R)(S)(S)-BF65 in turn suppresses Bcl-2 and MAPKs induced by MK-2206. (R)(S)(S)-BF65 and MK-2206 compensate each other leading to increased apoptosis and enhanced cytotoxicity, and may also suppress cancer cell invasion.

We demonstrated the controlled placement of a Ge quantum dot (QD) along with tunnel-junction engineering in a self-organized approach for the effective management of single charge tunneling. In this approach, a single-Ge-QD ( ~ 11 nm) self-aligning with nickel-polycide electrodes is realized by thermally oxidizing a SiGe nanorod that bridges a 15-nm-wide nanotrench in close proximity to electrodes via a spacer bilayer of Si3N4/SiO2. The fabricated Ge-QD single-hole transistor exhibits clear Coulomb oscillation and Coulomb diamond behaviors at T = 77 K-150 K, providing a way to analyze the electronic structure of the Ge QD.

We demonstrate a CMOS-compatible scheme, selective oxidation of SiGe pillars, for creating well-organized 3-D Ge quantum dot (QD) array by guiding QDs migration along the oxidation path and thus placing them on targeted locations where the ultimate oxidation occurs. Stacked QDs exhibit tunable luminescence over the visible and possess low thermal conductivity, showing promise for nanophotonic and energy conversion devices.

Controlled heterogeneous nucleation and growth of Ge quantum dots (QDs) are demonstrated on SiO_2/Si_3N_4 substrates by means of a novel fabrication process of thermally oxidizing nanopatterned SiGe layers. The otherwise random self-assembly process for QDs is shown to be strongly influenced by the nanopatterning in determining both the location and size of the QDs. Ostwald ripening processes are observed under further annealing at the oxidation temperature. Both nanopattern oxidation and Ostwald ripening offer additional mechanisms for lithography for controlling the size and placement of the QDs.

Trigate Si nanowire (NW) MOSFETs have been fabricated and characterized at temperature between 77 and 300 K in the dark and under light pumping. The NW width W and height H, the gate length Lg, and the gate oxide thickness tox, respectively, were 7-25, 16, 34-52, and 7 nm. The interesting aspects of Si NW MOSFETs with W/Lg = 25 nm /52 nm, 24 nm/34 nm, 7 nm/47 nm, and 10 nm/37 nm measured at low drain voltage are that the drain current exhibited not only inverse temperature dependence in strong accumulation but also clear current plateaus/oscillations near the threshold regime at temperature up to 300 K. Notably, such current plateaus diminished or were invisible in the device of W/Lg = 24 nm/42 nm. The observed current behaviors are inferred from the interplay of quantum interference and intersubband scattering effects. Additional current plateaus due to photogenerated excitons were also observed in the studied devices, evidencing photoexcitation effects on quantum transports through a Si NW.

A new bandpass shielding enclosure (BPSE) made by etching the apertures of a periodic hexagon array on its top and bottom surfaces is proposed for modern portable digital devices having wireless communication functions. The BPSE is required to provide high transmittance at the specified communication band and high shielding effectiveness outside this band, and to have little influence on the radiation characteristics of an internal antenna located inside the enclosure. All three required features are difficult to achieve simultaneously. A prototype of the BPSE was built and studied. Both the simulated and measured results obtained show the promising performance of the BPSE and its potential in practical applications. © 2007 Wiley Periodicals, Inc. Microwave Opt Technol Lett 50: 15–18, 2008; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/mop.22978

Glycolysis machinery regulates cancer cell behavior. However, the roles of these glycolysis enzymes in oral squamous cell carcinoma (OSCC) progression remain unknown.Fructose-bisphosphate aldolase C (ALDOC) expression in OSCC patients and cell lines was detected using quantitative real-time polymerase chain reaction (PCR). The functions of ALDOC in migration and invasion were determined using gain and loss of function approaches. An orthotopic OSCC animal model was performed to investigate the effects of ALDOC on metastasis and tumorigenesis in vivo.ALDOC expression is negatively significantly correlated with clinical outcome and cell migration in vitro and in vivo. ALDOC blocks adenosine triphosphate generation and lactate production, and mutation constructs of Arg42 and Lys146 functionally restore ALDOC-inhibited cell migration and invasion.ALDOC functions as an OSCC prognosis marker clinically, and suppresses migration and invasion by its catalytic domain of Arg42 and Lys146. © 2015 Wiley Periodicals, Inc. Head Neck 38: E1075-E1085, 2016.

We report a unique, CMOS approach for the inclusion of size-tunable (7-50-nm), spherical Ge quantum dots (QDs) into gate stacks of Si MOS transistors, through selective oxidation of SiGe pillars over the buffer layer of Si3N4 on top of the Si substrate. The Ge-QD MOS phototransistors feature extremely low dark current densities (I off ∼ 0.27 pA/μm2), high I on /I off (>106), steep subthreshold swing (∼175 mV/dec at 300 K), superior external quantum efficiency (∼240%), and fast response time of 1.4ns under illumination of 850 nm, providing a core building block for high-performance Ge optical transducers for on-chip optical switches and transducers for Si-based optical interconnect applications. Most importantly, the detection wavelength of the Ge QD is tunable from near infrared to near ultraviolet by reducing the QD size from 50 to 7 nm, and the optimal photoresponsivity is tailored by the Ge QD size and the effective thickness of gate dielectrics.

A 7-year-old boy developed a left ventricular aneurysm with massive hemopericardium 3 years ago due to a fall from a fourth-floor window. He had mild neurological sequelae including cranial nerve III palsy and abnormal electroencephalography findings at that time. He had no chest pain until recently when he presented with chest tightness and abdominal pain for 2 days prior to admission. Chest X-ray showed marked cardiomegaly. Echocardiography revealed massive pericardial effusion and a large left ventricular aneurysm. The massive hemopericardium was surgically drained, and the aneurysm was resected under cardiopulmonary bypass. He was discharged uneventfully 1 week after operation. Because symptoms and signs can vary in patients with ventricular aneurysm, we strongly suggest a close clinical follow-up, preferably with chest X-ray or echocardiography, for patients experiencing a blunt chest trauma.

Interleukin (IL)-20 is a proinflammatory cytokine in the IL–10 family. IL–20 is associated with tumor promotion in the pathogenesis of oral, bladder, and breast cancer. However, little is known about the role of IL–20 in prostate cancer. We hypothesize that IL–20 promotes the growth of prostate cancer cells. Immunohistochemical staining showed that IL–20 and its receptors were expressed in human PC–3 and LNCaP prostate cancer cell lines and in prostate tumor tissue from 40 patients. In vitro, IL–20 upregulated N-cadherin, STAT3, vimentin, fibronectin, RANKL, cathepsin G, and cathepsin K, and increased the migration and colony formation of prostate cancer cells via activated p38, ERK1/2, AKT, and NF-κB signals in PC–3 cells. We investigated the effects of anti-IL–20 monoclonal antibody 7E on prostate tumor growth in vivo using SCID mouse subcutaneous and intratibial xenograft tumor models. In vivo, 7E reduced tumor growth, suppressed tumor-mediated osteolysis, and protected bone mineral density after intratibial injection of prostate cancer cells. We conclude that IL–20 is involved in the cell migration, colony formation, and tumor-induced osteolysis of prostate cancer. Therefore, IL–20 might be a novel target for treating prostate cancer.

Interleukin (IL)-20, a proinflammatory cytokine of the IL-10 family, is involved in acute and chronic renal failure. The aim of this study was to elucidate the role of IL-20 during diabetic nephropathy development. We found that IL-20 and its receptor IL-20R1 were upregulated in the kidneys of mice and rats with STZ-induced diabetes. In vitro, IL-20 induced MMP-9, MCP-1, TGF-β1 and VEGF expression in podocytes. IL-20 was upregulated by hydrogen peroxide, high-dose glucose and TGF-β1. In addition, IL-20 induced apoptosis in podocytes by activating caspase-8. In STZ-induced early diabetic nephropathy, IL-20R1-deficient mice had lower blood glucose and serum BUN levels and a smaller glomerular area than did wild-type controls. Anti-IL-20 monoclonal antibody (7E) treatment reduced blood glucose and the glomerular area and improved renal functions in mice in the early stage of STZ-induced diabetic nephropathy. ELISA showed that the serum IL-20 level was higher in patients with diabetes mellitus than in healthy controls. The findings of this study suggest that IL-20 induces cell apoptosis of podocytes and plays a role in the pathogenesis of early diabetic nephropathy. Serious kidney damage often found in type 1 and type 2 diabetes has been linked to the natural signaling molecule interleukin-20 (IL-20). Ming-Shi Chang and colleagues at the National Cheng Kung University in Taiwan found increased levels of both IL-20 and its receptor molecule in mice and rats with chemically induced diabetes. They also found that IL-20 induced changes in gene activity, leading to cell death in cultured specialized kidney cells known as podocytes. Patients with diabetes were also shown to have increased IL-20 levels. Treating diabetic mice with an antibody that bound to and interfered with the activity of IL-20 improved kidney function and reduced biochemical indicators of diabetes. Understanding the mechanism of IL-20 involvement in this common complication of diabetes could help devise treatments to prevent or limit the damage.

We demonstrated a novel, self-aligned gate-stack heterostructure of Ge-quantum dot (QD)/SiO 2 /SiGe-shell on Si with superior interfacial properties in a single step of selective oxidation of a SiGe pillar over a Si 3 N 4 buffer layer on Si substrate. Ge metal-oxide-semiconductor (MOS) capacitors exhibit a quite low interface trap density on the order of 1011 cm−2eV−1, and Ge n-MOSFETs show good turn on and off features with a subthreshld slope of 175 mV/dec and I on /I off > 106.

Liquid-phase and solid-phase extractions (SPE) in combination with a simple micellar electrokinetic chromatography (MEKC) method were used to investigate human very low-density lipoprotein (VLDL) lipids for two healthy donors. At absorbance 200 nm, the effective mobilities and peak areas of the MEKC profiles showed good reproducibility and precisions. A major peak and several minor peaks appeared for the total lipids of native VLDL, but both the peak numbers and areas reduced for the in vitro oxidized VLDL. Two chloroform and two methanol fractions were obtained from SPE of VLDL total lipids. Significant differences were observed for the first methanol fraction between native and in vitro oxidized VLDL lipids. The first methanol fraction showed a major peak and several minor peaks for native VLDL, but both the peak numbers and areas reduced for oxidized VLDL. Oxidation of VLDL caused decomposition of lipids, and thus the reduction of peak numbers and areas.

A simple capillary zone electrophoresis (CZE) method was used to characterize human very low-density lipoprotein (VLDL) particles for four healthy donors. One major peak was observed for native, in vitro oxidized and glycated VLDL particles. The effective mobilities and peak areas of the capillary electrophoresis (CE) profiles showed good reproducibility and precision. The mobility of the oxidized VLDL peak was higher than that of the native VLDL. The mobility of the glycated VLDL peak was similar to that of the native VLDL. Phospholipids isolated from VLDL particles were analyzed by our recently developed micellar electrokinetic chromatography (MEKC) with a high-salt stacking method. At absorbance 200 nm, the native VLDL phospholipids showed a major peak and a minor peak for each donor. For oxidized VLDL phospholipids, the area of the major peak reduced for three donors, possibly due to phospholipid decomposition. For glycated VLDL phospholipids, the peak mobilities were more positive than native VLDL phospholipids for two donors, possibly due to phospholipid-linked advanced glycation end products (AGEs). Very interestingly, at absorbance 234 nm, the major peak of oxidized VLDL phospholipids was resolved as two peaks for each donor, possibly due to conjugated dienes formed upon oxidation.

A single Ge quantum-dot (~10 nm) forms and self-aligns with source/drain electrodes via SiO2 tunneling barriers using thermal oxidation of a SiGe-on-insulator nanowire. Thereby, a Ge single-hole transistor with self-aligned electrodes is experimentally realized based on FinFET technology and features with clear Coulomb staircase/negative differential conductance and large Coulomb-blockade oscillation behaviors at room temperature. This work provides a simple approach to alleviate this nanofabrication bottleneck and thereby reduce series resistances and increase design freedom for SETs.

A single electron transistor (SET) is an ultimate scheme of electronic devices for the purpose of controlling current with one charge precision based on Coulomb blockade effect. A SET could be used as a highly sensitive electrometer and might provide great potential applications for quantum information technology. For RT operation, the size of a Si-based QD should be less than 10 nm to prevent errors caused by thermal fluctuation. Nevertheless, control of nanometer-scaled thickness, area, and volume is not easy even when state of the art lithography and/or self-organization techniques are used. The solution we propose to alleviate this problem is to form Ge QDs by selective oxidation of Si1-xGexSi-on-insulator (SOI) (Li et al., 2004). Using this method, Ge QDs are comparatively uniform and thermodynamically stable since Ge QDs are confined by the insulating layers. The proposed process is compatible to CMOS technology and can be easily adapted in the fabrication of embedded circuits

We reported experimental observations of strong quantum confinement and coulomb blockade effects in germanium (Ge) quantum dots (QDs)/SiO/sub 2/ system. With a CMOS-compatible method, nanometer-scale Ge QDs (less than 10 nm) could be controllably formed for novel optoelectronic device applications such as single-electron transistors (SETs) as well as light emitter or detectors. Distinguishable photoemission from Ge QDs and relevant blueshifts of the emission peaks are observed from room-temperature cathodoluminescence spectra. Ge QD SETs were also experimentally realized with a large single-electron addition energy and an energy level separation of 125 meV and 50 meV, respectively.

Semiconductor Ge quantum-dot (QD) thermometry has been demonstrated based on extraordinary temperature-dependent oscillatory differential conductance (GD) characteristics of Ge-QD single-hole transistors (SHTs) in the few-hole regime. Full-voltage width-at-half-minimum, V1/2, of GD valleys appears to be fairly linear in the charge number (n) and temperature within the QD in a relationship of eV1/2 ≅ (1 − 0.11n) × 5.15kBT, providing the primary thermometric quantity. The depth of GD valley is also proportional to charging energy (EC) and 1/T via ΔGD ≅ EC/9.18kBT, providing another thermometric quantity. This experimental demonstration suggests our Ge-QD SHT offering effective building blocks for nanothermometers over a wide temperature range with a detection temperature as high as 155 K in a spatial resolution less than 10 nm and temperature accuracy of sub-kelvin.

The purpose of this study was to study the morphology and cytokeratin expression in the epithelia of pterygia. Impression cytology and immunohistochemical staining with antikeratin antibodies were performed in 32 eyes of 16 patients with pterygia. TUNEL stain and electron microscopy were also performed in surgical specimens of pterygium. Squamous metaplasia-like epithelial cells were found in all specimens of impression cytology, especially in the head part. These specimens had positive immunostaining by antipancytokeratin antibodies, but not by anti-K12 AK2 mAb. Goblet cells were found around the area of these abnormal epithelial cells. TUNEL-positive cells were found in the epithelia of the pterygial head, but not in the body of pterygia and normal conjunctiva. The expressional patterns of keratin by these epithelial cells of pterygia are consistent with the notion that they are derived from conjunctival epithelium and mimic the process of squamous metaplasia.