Al12Co4: a pioneering heterometallic aluminum oxo cluster with surface-exposed Co sites for the oxygen evolution reaction.

We report an unprecedented heterometallic aluminum oxo cluster (AlOC) containing four surface-exposed CoII sites, designated as Al12Co4, protected by four t-butylcalix[4]arene (TBC[4]) molecules. The Al12Co4 nanocluster represents a significant advancement on multiple innovative fronts. First, it stands as an pioneering example of an AlIII-based metallocalixarene nanocluster. It is also the first instance of heterometallic AlOCs shielded by macrocyclic ligands. Notably, this cluster also holds the distinction of being the highest nuclearity Al-Co bimetallic nanocluster known to date. Additionally, by depositing Al12Co4 on carbon nanotubes (CNTs) as a supported catalyst, we investigated its electrocatalytic performance for the oxygen evolution reaction in alkaline media. To reach a 10 mA cm-2 current density in alkaline solution, the Al12Co4@CNT electrode needs overpotential as low as 320 mV.

Sirtuin 3 Ameliorates Lung Senescence and Improves Type II Alveolar Epithelial Cell Function by Enhancing the FoxO3a-Dependent Antioxidant Defense Mechanism.

Lung aging alters the intrinsic structure of the lung and pulmonary surfactant system and increases the mortality and morbidity due to respiratory diseases in elderly individuals. We hypothesized that lung aging results from an insufficiency of type II alveolar epithelial cells (AECIIs) in the lung tissue. Sirtuin 3 (SIRT3) is a member of the sirtuin family of proteins that promote longevity in many organisms. Increased SIRT3 expression has been linked to an extended life span in humans. Hence, we speculated that the overexpression of SIRT3 may help to ameliorate lung senescence and improve AECII function. AECIIs were isolated from young and old patients with pneumothorax caused by pulmonary bullae. The expression of SIRT3, manganese superoxide dismutase, and catalase, as well as cell function and senescence indicators of young and old AECIIs, was measured before and after SIRT3 overexpression. After SIRT3 overexpression, the aged state of old AECIIs improved, and antiapoptotic activity, proliferation, and secretion were dramatically enhanced. Surfactant protein C (SPC), which is secreted by AECIIs, reduces alveolar surface tension, repairs the alveolar structure, and regulates inflammation. SPC deficiency in patients is associated with increased inflammation and delayed repair. SIRT3 deacetylated forkhead box O3a, thereby protecting mitochondria from oxidative stress and improving cell function and the senescent state of old AECIIs. These findings provide a possible direction for aging-delaying therapies and interventions for diseases of the respiratory system.

Evidence for the existence of CD34+ angiogenic stem cells in human first-trimester decidua and their therapeutic for ischaemic heart disease.

Stem cell transplantation is nearly available for clinical application in the treatment of ischaemic heart disease (IHD), where it may be joined traditional methods (intervention and surgery). The angiogenic ability of seed cells is essential for this applicability. The aim of this study was to reveal the presence of CD34+ angiogenic stem cells in human decidua at the first trimester and to use their strong angiogenic capacity in the treatment of IHD. In vitro, human decidual CD34+ (dCD34+ ) cells from the first trimester have strong proliferation and clonality abilities. After ruling out the possibility that they were vascular endothelial cells and mesenchymal stem cells (MSCs), dCD34+ cells were found to be able to form tube structures after differentiation. Their angiogenic capacity was obviously superior to that of bone marrow mesenchymal stem cells (BMSCs). At the same time, these cells had immunogenicity similar to that of BMSCs. Following induction of myocardial infarction (MI) in adult rats, infarct size decreased and cardiac function was significantly enhanced after dCD34+ cell transplantation. The survival rate of cells increased, and more neovasculature was found following dCD34+ cell transplantation. Therefore, this study confirms the existence of CD34+ stem cells with strong angiogenic ability in human decidua from the first trimester, which can provide a new option for cell-based therapies for ischaemic diseases, especially IHD.

A de novo DDX3X Variant Is Associated With Syndromic Intellectual Disability: Case Report and Literature Review.

De novo DDX3X variants account for 1%-3% of intellectual disability (ID) in females and have been occasionally reported in males. Here, we report a female patient with severe ID and various other features, including epilepsy, movement disorders, behavior problems, sleep disturbance, precocious puberty, dysmorphic features, and hippocampus atrophy. With the use of family-based exome sequencing, we identified a de novo pathogenic variant (c.1745dupG/p.S583*) in the DDX3X gene. However, our patient did not present hypotonia, which is considered a frequent clinical manifestation associated with DDX3X variants. While hand stereotypies and sleep disturbance have been occasionally associated with the DDX3X spectrum, hippocampus atrophy has not been reported in patients with DDX3X-related ID. The investigation further expands the phenotype spectrum for DDX3X variants with syndromic intellectual disability, which might help to improve the understanding of DDX3X-related intellectual disability or developmental delay.

SIRT3 Transfection of Aged Human Bone Marrow-Derived Mesenchymal Stem Cells Improves Cell Therapy-Mediated Myocardial Repair.

Sirtuin 3 (SIRT3) is a deacetylase important for antioxidant protection, cell longevity, and aging. We hypothesized that SIRT3 improve oxidative resistance of aged cells and improve cell therapy in aged patients. In vitro, the proliferation and oxidative resistance of human mesenchymal stem cells (hMSCs) significantly declined with age. The expression and activity of antioxidant enzymes, including catalase (CAT) and manganese superoxide dismutase (MnSOD), increased after transfection of SIRT3 in hMSCs from older donors (O-hMSCs). The protein level of Forkhead box O3a (FOXO3a) in nucleus increased after SIRT3 overexpression. The antioxidant capacity of O-hMSCs increased after SIRT3 overexpression. 3-Amino-1,2,4-triazole (3-AT, CAT inhibitor) or diethyldithiocarbamate (DETC, SOD inhibitor) that was used to inhibit CAT or SOD activity significantly blocked the antioxidant function of SIRT3. When two inhibitors were used together, the antioxidant function of SIRT3 almost disappeared. Following myocardial infarction and intramyocardial injections of O-hMSCs in rats in vivo, the survival rate of O-hMSCs increased by SIRT3 transfection. The cardiac function of rats was improved after SIRT3-overexpressed O-hMSC transplantation. The infarct size, collagen content, and expression levels of matrix metalloproteinase 2 (MMP2) and MMP9 decreased. Besides, the protein level of vascular endothelial growth factor A and vascular density increased after cell transplantation with SIRT3-modified O-hMSCs. These results indicate that damage resistance of hMSCs decline with age and SIRT3 might protect O-hMSCs against oxidative damage by activating CAT and MnSOD through transferring FOXO3a into nucleus. Meanwhile, the therapeutic effect of aged hMSC transplantation can be improved by SIRT3 overexpression.

Sirtuin3 protects aged human mesenchymal stem cells against oxidative stress and enhances efficacy of cell therapy for ischaemic heart diseases.

Sirtuin3 (SIRT3) is associated with oxidative stress and lifespan. However, the possible mechanisms underlying its influence are unknown. We hypothesized that SIRT3 increases the antioxidant capacity of aged cells and improves the efficacy of human mesenchymal stem cell (hMSC) therapy for ischaemic heart diseases in aged patients. In vitro, the antioxidant capacity of old hMSCs (O-hMSCs) was increased after SIRT3 overexpression using a gene transfection technique, while the antioxidant capacity of young hMSCs (Y-hMSCs) was decreased by SIRT3 silencing. The levels of forkhead box O3a (FoxO3a) in the nucleus, and antioxidant enzymes Mn-superoxide dismutase (MnSOD) and catalase (CAT) increased in SIRT3-overexpressed O-hMSCs while they decreased in SIRT3-silenced Y-hMSCs after oxidative stress. Following myocardial infarction in adult rats in vivo, infarct size decreased and cardiac function was significantly enhanced after cell transplantation with SIRT3 overexpressed O-hMSCs. The number of apoptotic cells decreased and the survival rate of transplanted cells increased following SIRT3 overexpression in O-hMSCs. SIRT3 protects aged hMSCs against oxidative stress by positively regulating antioxidant enzymes (MnSOD and CAT) via increasing the expression of FoxO3a in the nucleus. The efficacy of aged hMSC transplantation therapy for ischaemic heart diseases can be improved by SIRT3 overexpression.

Identification and characterization of two novel C-type lectins from the larvae of housefly, Musca domestica L.

Lectins and antimicrobial peptides (AMPs) are widely distributed in various insects and play crucial roles in primary host defense against pathogenic microorganisms. Two AMPs (cecropin and attacin) have been identified and characterized in the larvae of housefly. In this study, two novel C-type lectins (CTLs) were obtained from Musca domestica, while their agglutinating and antiviral properties were evaluated. Real-time PCR analysis showed that the mRNA levels of four immune genes (MdCTL1, MdCTL2, Cecropin, and Attacin) from M. domestica were significantly upregulated after injection with killed Gram-negative Escherichia coli. Moreover, purified MdCTL1-2 proteins can agglutinate E. coli and Staphylococcus aureus in the presence of calcium ions, suggesting their immune function is Ca2+ dependent. Sequence analysis indicated that typical WND and QPD motifs were found in the Ca2+ -binding site 2 of carbohydrate recognition domain from MdCTL1-2, which was consistent with their agglutinating activities. Subsequently, antiviral experiments indicated that MdCTL1-2 proteins could significantly reduce the infection rate of Spodoptera frugiperda 9 cells by the baculovirus Autographa californica multicapsid nucleopolyhedrovirus, indicating they might play important roles in insect innate immunity against microbial pathogens. In addition, MdCTL1-2 proteins could effectively inhibit the replication of influenza H1 N1 virus, which was similar to the effect of ribavirin. These results suggested that two novel CTLs could be considered a promising drug candidate for the treatment of influenza. Moreover, it is believed that the discovery of the CTLs with antiviral effects in M. domestica will improve our understanding of the molecular mechanism of insect immune response against viruses.

Genome-wide dissection of heterosis for yield traits in two-line hybrid rice populations.

Heterosis has been widely utilized in agriculture and is important for world food safety. Many genetic models have been proposed as mechanisms underlying heterosis during the past century, yet more evidence is needed to support such models. To investigate heterosis in two-line hybrid rice, we generated a partial diallel crossing scheme, which consisted of approximately 500 F1 hybrids derived from 14 male sterile lines and 39 restorer lines. In this population, increased panicle number played the most important role in yield heterosis of hybrid rice. Genome-wide association studies identified many QTLs related to the yield traits of F1 hybrids, better paternal heterosis and special combining ability. Relevant genes, including Hd3a, qGL3, OsmiR156h, and LAX2, were identified as candidates within these QTLs. Nearly forty percent of the QTLs had only two genotypes in the F1 hybrids, mainly because the maternal lines were under intense selective pressure. Further analysis found male sterile lines and restorer lines made different superior allele contributions to F1 hybrids, and their contributions varied among different traits. These results extend our understanding of the molecular basis of heterosis in two-line hybrid rice.

Suppression of miR-34a Expression in the Myocardium Protects Against Ischemia-Reperfusion Injury Through SIRT1 Protective Pathway.

MicroRNA-34a (miR-34a) is expressed in the myocardium and expression is altered after myocardial injury. We investigated the effects of miR-34a on heart function after ischemia-reperfusion (IR) injury. Cardiomyocytes were isolated from neonatal rat hearts and simulated IR injury was induced in vitro. Following IR injury in rats, infarct size was measured and left ventricular (LV) function was evaluated using echocardiography. Protein expression of silent information regulator 1 (SIRT1), acetylated p53 (ac-p53), Bcl-2 and Bax, and miR-34a and SIRT1 gene levels were analyzed. miR-34a overexpression exacerbated myocardial injury by increasing apoptosis and infarct size and decreasing LV function. Suppression of miR-34a attenuated myocardial IR injury. SIRT1 was negatively regulated by miR-34a and the expression of downstream genes, such as ac-p53, Bcl-2, and Bax were altered correspondingly. Increased expression of miR-34a aggravates injury after IR; miR-34a suppression therapy may represent a new line of treatment for myocardial IR injury.

MOLECULAR CHARACTERIZATION OF AUTOPHAGY-RELATED GENE 5 FROM Spodoptera exigua AND EXPRESSION ANALYSIS UNDER VARIOUS STRESS CONDITIONS.

Autophagy is not only involved in development, but also has been proved to attend immune response against invading pathogens. Autophagy protein 5 (ATG5) is an important autophagic protein, which plays a crucial role in autophagosome elongation. Although ATG5 has been well studied in mammal, yeast, and Drosophila, little is known about ATG5 in lepidopteran insects. We cloned putative SeAtg5 gene from Spodoptera exigua larvae by the rapid amplification of cDNA ends method, and its characteristics and the influences of multiple exogenous factors on its expression levels were then investigated. The results showed that the putative S. exigua SeATG5 protein is highly homologous to other insect ATG5 proteins, which has a conserved Pfm domain and multiple phosphorylation sites. Next, fluorescence microscope observation showed that mCherry-SeATG5 was distributed in both nucleus and cytoplasm of Spodoptera litura Sl-HP cells and partially co-localized with BmATG6-GFP, but it almost has no significant co-localization with GFP-HaATG8. Then, the Western blot analysis demonstrated that GFP-SeATG5 conjugated with ATG12. Moreover, real-time PCR revealed that its expression levels significantly increased at the initiation of pupation and the stage of adult. In addition, the expression levels of SeAtg5 can be enhanced by the starvation, UV radiation, and infection of baculovirus and bacterium. However, the expression levels of SeAtg5 decreased at 24 h post treatments in all these treatments except in starvation. These results suggested that SeATG5 might be involved in response of S. exigua under various stress conditions.

Inhibitory effect of arsenic trioxide on neuronal migration in vitro and its potential molecular mechanism.

Primary neuron cultures were established from the brains of neonatal rats and the effects of arsenic trioxide (As2O3) on the migration of neurons and the potential mechanism of As2O3 were investigated. Boyden chamber assay was used to detect the effect of AS2O3 on neuronal migration. Matrix metalloproteinase-2 (MMP-2) and MMP-9 RNA expression and doublecortin (DCX) protein expression were measured. Neuronal migration ability was significantly lower in the 20 µmol/L group compared with the other three groups (all p < 0.001). The expression of both MMP-2 and MMP-9 was significantly inversely correlated with As2O3 concentration. The expression of DCX was significantly higher in the control group compared with the other three groups (all p ≤ 0.003). Thus, the inhibitory effect of As2O3 on the migration of primary neurons might be related to the reduction in MMP-2 and MMP-9 activities and decrease in ß-actin and DCX expression.

Decreased SIRT3 in aged human mesenchymal stromal/stem cells increases cellular susceptibility to oxidative stress.

Sirtuin3 (SIRT3) is an important member of the sirtuin family of protein deacetylases that is localized to mitochondria and linked to lifespan extension in organisms ranging from yeast to humans. As aged cells have less regenerative capacity and are more susceptible to oxidative stress, we investigated the effect of ageing on SIRT3 levels and its correlation with antioxidant enzyme activities. Here, we show that severe oxidative stress reduces SIRT3 levels in young human mesenchymal stromal/stem cells (hMSCs). Overexpression of SIRT3 improved hMSCs resistance to the detrimental effects of oxidative stress. By activating manganese superoxide dismutase (MnSOD) and catalase (CAT), SIRT3 protects hMSCs from apoptosis under stress. SIRT3 expression, levels of MnSOD and CAT, as well as cell survival showed little difference in old versus young hMSCs under normal growth conditions, whereas older cells had a significantly reduced capacity to withstand oxidative stress compared to their younger counterparts. Expression of the short 28 kD SIRT3 isoform was higher, while the long 44 kD isoform expression was lower in young myocardial tissues compared with older ones. These results suggest that the active short isoform of SIRT3 protects hMSCs from oxidative injury by increasing the expression and activity of antioxidant enzymes. The expression of this short isoform decreases in cardiac tissue during ageing, leading to a reduced capacity for the heart to withstand oxidative stress.

PIM-1 modulates cellular senescence and links IL-6 signaling to heterochromatin formation.

Cellular senescence is a stable state of proliferative arrest that provides a barrier against malignant transformation and contributes to the antitumor activity of certain chemotherapies. Unexpectedly, we found that the expression of proto-oncogene PIM-1, which can promote tumorigenesis, is induced at transcriptional level during senescence. Inhibition of PIM-1 alleviated both replicative and oncogene-induced senescence. Conversely, ectopic expression of PIM-1 resulted in premature senescence. We also revealed that PIM-1 interacts with and phosphorylates heterochromatin protein 1γ (HP1γ) on Ser93. This PIM-1-mediated HP1γ phosphorylation enhanced HP1γ's capacity to bind to H3K9me3, resulting in heterochromatin formation and suppression of proliferative genes, such as CCNA2 and PCNA. Analysis of the mechanism underlying the up-regulation of PIM-1 expression during senescence demonstrated that IL-6, a critical regulator of cellular senescence, is responsible for PIM-1 induction. Our study demonstrated that PIM-1 is a key component of the senescence machinery that contributes to heterochromatin formation. More importantly, we demonstrated that PIM-1 is also a direct target of IL-6/STAT3 signaling and mediates cytokine-induced cellular senescence.

Expression of the tissue inhibitor of metalloproteinase-3 by transplanted VSMCs modifies heart structure and function after myocardial infarction.

OBJECTIVES: Extracellular matrix (ECM) remodelling is a critical aspect of cardiac remodelling following myocardial infarction. Tissue inhibitors of metalloproteinases (TIMPs) are physiological inhibitors of matrix metalloproteinases (MMPs) that degrade the ECM proteins. TIMP-3 is highly expressed in the heart and is markedly downregulated in patients with ischaemic cardiomyopathy. Cell-based gene therapy can enhance the effects of cell transplantation by temporally and spatially regulating the release of the gene product. The purpose of this study was to investigate the role of TIMP-3 gene-transfected vascular smooth muscle cells (VSMCs) in modifying heart structure and function in rats when transplanted 3days after myocardial infarction (MI). METHODS: Anesthetised rats were subjected to coronary artery ligation followed 3days later by thoracotomy and transplantation of TIMP-3 gene-transfected VSMCs, untransfected VSMCs or medium injected directly into the ischaemic myocardium. We assessed left ventricular structure and function by echocardiography and morphometry, and measured the levels of myocardial matrix metalloproteinase-2 and -9 (MMP-2, MMP-9), TIMP-3 and tumour necrosis factor-α (TNF-α) at 4weeks post-myocardial infarction. RESULTS: Transplantation of TIMP-3 gene-transfected VSMCs and untransfected VSMCs significantly decreased scar expansion and ventricular dilatation 25days post-transplantation (4weeks after MI). MMPs and TNF-α levels were reduced in the transplantation groups when compared to the group that was given an injection of medium only. Transplantation of TIMP-3 gene-transfected VSMCs was more effective in preventing progressive cardiac dysfunction, ventricular dilatation and in reducing MMP-2, MMP-9 and TNF-α levels when compared to the transplantation of untransfected VSMCs. CONCLUSIONS: TIMP-3 gene transfection was associated with attenuated left ventricular dilation and recovery of systolic function after MI compared with the control. TIMP-3 transfection enhanced the effects of transplanted VSMCs in rats by inhibiting matrix degradation and inflammatory cytokine expression, leading to improved myocardial remodelling.

A minority subpopulation of CD133(+) /EGFRvIII(+) /EGFR(-) cells acquires stemness and contributes to gefitinib resistance.

AIMS: To study the contribution of epidermal growth factor receptor variant III (EGFRvIII) to glioblastoma multiforme (GBM) stemness and gefitinib resistance. METHODS: CD133(+) and CD133(-) cells were separated from EGFRvIII(+) clinical specimens of three patients with newly diagnosed GBM. Then, RT-PCR was performed to evaluate EGFRvIII and EGFR expression in CD133(+) and CD133(-) cells. The tumorigenicity and stemness of CD133(+) cells was verified by intracranial implantation of 5 × 10(3) cells into immunodeficient NOD/SCID mice. Finally, cells were evaluated for their sensitivity to EGFR tyrosine kinase inhibition by gefitinib. RESULTS: RT-PCR results showed that the sorted CD133(+) cells expressed EGFRvIII exclusively, while the CD133(-) cells expressed both EGFRvIII and EGFR. At 6-8 weeks postimplantation, CD133(+) /EGFRvIII(+) /EGFR(-) cells formed intracranial tumors. Cell counting kit-8 results showed that the IC50 values of the three isolated EGFRvIII(+) cell lines treated with gefitinib were 14.44, 16.00, and 14.66 µM, respectively, whereas the IC50 value of an isolated EGFRvIII(-) cell line was 8.57 µM. CONCLUSIONS: EGFRvIII contributes to the stemness of cancer stem cells through coexpression with CD133 in GBMs. Furthermore, CD133(+) /EGFRvIII(+) /EGFR(-) cells have the ability to initiate tumor formation and may contribute to gefitinib resistance.

Tissue inhibitor of matrix metalloproteinase-3 or vascular endothelial growth factor transfection of aged human mesenchymal stem cells enhances cell therapy after myocardial infarction.

Mesenchymal stem cell (MSC) transplantation has been proposed as a potential therapeutic approach for ischemic heart disease, but the regenerative capacity of these cells decreases with age. In this study, we genetically engineered old human MSCs (O-hMSCs) with tissue inhibitor of matrix metalloproteinase-3 (TIMP3) and vascular endothelial growth factor (VEGF) and evaluated the effects on the efficacy of cell-based gene therapy in a rat myocardial infarction (MI) model. Cultured O-hMSCs were transfected with TIMP3 (O-TIMP3) or VEGF (O-VEGF) and compared with young hMSCs (Y-hMSCs) and non-transfected O-hMSCs for growth, clonogenic capacity, and differentiation potential. In vivo, rats were subjected to left coronary artery ligation with subsequent injection of Y-hMSCs, O-hMSCs, O-TIMP3, O-VEGF, or medium. Echocardiography was performed prior to and at 1, 2, and 4 weeks after MI. Myocardial levels of matrix metalloproteinase-2 (MMP2), MMP9, TIMP3, and VEGF were assessed at 1 week. Hemodynamics, morphology, and histology were measured at 4 weeks. In vitro, genetically modified O-hMSCs showed no changes in growth, colony formation, or multi-differentiation capacity. In vivo, transplantation with O-TIMP3, O-VEGF, or Y-hMSCs increased capillary density, preserved cardiac function, and reduced infarct size compared to O-hMSCs and medium control. O-TIMP3 and O-VEGF transplantation enhanced TIMP3 and VEGF expression, respectively, in the treated animals. O-hMSCs genetically modified with TIMP3 or VEGF can increase angiogenesis, prevent adverse matrix remodeling, and restore cardiac function to a degree similar to Y-hMSCs. This gene-modified cell therapy strategy may be a promising clinical treatment to rejuvenate stem cells in elderly patients.

Inhibiting matrix metalloproteinase by cell-based timp-3 gene transfer effectively treats acute and chronic ischemic cardiomyopathy.

After a myocardial infarction (MI), an increase in the cardiac ratio of matrix metalloproteinases (MMPs) relative to their inhibitors (TIMPs) causes extracellular matrix modulation that leads to ventricular dilatation and congestive heart failure. Cell therapy can mitigate these effects. In this study, we tested whether increasing MMP inhibition via cell-based gene transfer of Timp-3 further preserved ventricular morphometry and cardiac function in a rat model of MI. We also measured the effect of treatment timing. We generated MI (coronary artery ligation) in adult rats. Three or 14 days later, we implanted medium (control) or vascular smooth muscle cells transfected with empty vector (VSMCs) or Timp-3 (C-TIMP-3) into the peri-infarct region (n = 15-24/group). We assessed MMP-2 and -9 expression and activity, TIMP-3, and TNF-α expression, cell apoptosis, infarct size and thickness, ventricular morphometry, and cardiac function (by echocardiography). Relative to medium, VSMCs delivered at either time point significantly reduced cardiac expression and activity of MMP-2 and -9, reduced expression of TNF-α, and increased expression of TIMP-3. Cell therapy also reduced apoptosis and scar area, increased infarct thickness, preserved ventricular structure, and reduced functional loss. All these effects were augmented by C-TIMP-3 treatment. Survival and cardiac function were significantly greater when VSMCs or C-TIMP-3 were delivered at 3 (vs. 14) days after MI. Upregulating post-MI cardiac TIMP-3 expression via cell-based gene therapy contributed additional regulation of MMP, TIMP, and TNF-α levels, thereby boosting the structural and functional effects of VSMCs transplanted at 3 or 14 days after an MI in rats. Early treatment may be superior to late, though both are effective.

Simultaneous characterization of the shape and refractive index of transparent living cells by an optical aperture.

We report a method of using optical aperture diffraction to simultaneously detect the image and the refractive index of a living cell. By simulation, it is found that, when a suitable gap is introduced between the cell and the aperture, the image of the cell on the detection plane can be amplified hundreds to thousands of times, and a limit of detection of 3e-4 to 9e-5 can be reached for the refractive index of the cell. Experiments show that this method is feasible to realize, but the achievement of such a detection system is yet to be proved.

Fabrication of gold nanocrescents by angle deposition with nanosphere lithography for localized surface plasmon resonance applications.

The gold nanostructures fabricated on a substrate yield localized surface plasmon resonance. We describe the fabrication and characterization of nanocrescents on a silicon substrate, which are fabricated by depositing a gold film at an oblique angle through nanosphere lithography. Following the etching of the gold perpendicular to the substrate and the removal of the nanospheres by dissolution, nanocrescents with fine nanostructures are generated. By varying the deposition angle of the gold film from 0 degrees to 72 degrees , nanorings, 2D and 3D nanocrescents can be obtained. During the nanocrescent fabrication, we also compared the deposition angle difference between the e-beam and thermal evaporators for oblique depositions of the gold. The 3D nanocrescents fabricated in our experiments are expected to have improved sensitivity in localized surface plasmon resonance measurements when compared to the previously reported 2D nanocrescents, which enable broader biosensor applications. Simulations of the profiles of these 3D nanocrescents using solid geometry show good consistency with the fabricated ones.

Algorithm and simulation for analysis of bio-images obtained by aperture diffraction based optical MEMS.

This paper proposes a novel method to detect transparent living cells in a transparent microfluidic chamber by optical diffraction of an aperture or an aperture array. Through the analysis of the far-field diffraction pattern, one of the parameters of the cells, including the size, refractive index, or position, can be extracted by the analysis software developed in this paper. Calculations are carried out to discuss the key issues of this MEMS device, and our simulation is verified by diffraction patterns of transparent microparticles on fabricated apertures, recorded via a digital camera.