Molecularly imprinted polymer coating-assisted CsPbBr3 perovskite quantum dots/TiO2 inverse opal heterojunctions for the photoelectrochemical detection of cholesterol.

Photoelectrochemical sensors have outstanding advantages including high sensitivity and miniaturization for outdoor use. Recently, perovskite quantum dots have attracted significant attention due to their high photoluminescence quantum yield. Nonetheless, there is still a strong need to improve their performance in challenging aqueous biological applications. In this paper, based on the molecularly imprinted polymer encapsulation of CsPbBr3 perovskite quantum dot/TiO2 inverse opal heterojunction structures, linear photoelectrochemical detection of cholesterol in aqueous solution was obtained without the involvement of an enzyme. The attenuation of photocurrent intensity under intermittent irradiation within 900 s (45 on/off cycles) was only 8.6%, demonstrating the superior stability of CsPbBr3 based sensor here. At the same time, the minimum detection limit of 1.22 × 10-9 mol L-1 in buffer conditions was lower than that reported for cholesterol photoelectric sensors. It has also been shown that the photoelectrochemical sensor of CsPbBr3 here outperformed that of CH3NH3PbBr3, which is another important member of the perovskite family. Finally, the proposed photoelectrochemical sensor platform was successfully applied in the determination of cholesterol in challenging serum with satisfactory recovery. The synergism among CsPbBr3 perovskite quantum dots, TiO2 inverse opal structure and imprinted polymer has led to greatly improved water stability, super selectivity and sensitivity, thus promoting the development of perovskite-based biological sensors.

Yellow Emission Obtained by Combination of Broadband Emission and Multi-Peak Emission in Garnet Structure Na2YMg2V3O12: Dy3+ Phosphor.

The fabrication and luminescent performance of novel phosphors Na2YMg2V3O12:Dy3+ were investigated by a conventional solid-state reaction method. Under near-UV light, the Na2YMg2V3O12 host self-activated and released a broad emission band (400-700 nm, with a peak at 524 nm) ascribable to charge transfer in the (VO4)3- groups. Meanwhile, the Na2YMg2V3O12:Dy3+ phosphors emitted bright yellow light within both the broad emission band of the (VO4)3- groups and the sharp peaks of the Dy3+ ions at 490, 582, and 663 nm at a quenching concentration of 0.03 mol. The emission of the as-prepared Na2YMg2V3O12:Dy3+ phosphors remained stable at high temperatures. The obtained phosphors, commercial Y2O3:Eu3+ red phosphors, and BaMgAl10O17:Eu2+ blue phosphors were packed into a white light-emitting diode (WLED) device with a near-UV chip. The designed WLED emitted bright white light with good chromaticity coordinates (0.331, 0.361), satisfactory color rendering index (80.2), and proper correlation to a color temperature (7364 K). These results indicate the potential utility of Na2YMg2V3O12:Dy3+ phosphor as a yellow-emitting phosphor in solid-state illumination.

A novel protein purification strategy mediated by the combination of CipA and Ssp DnaB intein.

Protein purification is an indispensable step in diverse fields of biological research or production process. Conventional purification methods including the affinity purification or the usage of self-aggregating tags suffered from many drawbacks such as the complicated steps, high cost and low efficiency. Moreover, the fusion tag usually had negative effects on the activity of the target protein. To address the above issues, here we propose a novel protein purification method which needs simple operation steps, and this method is mediated by the combination of CipA protein and a mini-intein (Synechocystis sp. PCC6803 DnaB, Ssp DnaB), depending on the assembly function of CipA and the self-cleavage function of Ssp DnaB. To realize the purification, CipA-DnaB-eGFP protein was expressed and assembled into protein crystalline inclusions (PCIs) in E. coli. Then, only cell lysis, cleavage and centrifugation steps were required to purify eGFP. Purified eGFP was in the supernatant with a purity of over 90%. The cleavage efficiency and the yield of eGFP reached 51.96% and 13.99 ±â€¯0.88 mg/L fermentation broth, respectively. Furthermore, to broaden the application of this approach, three other proteins which were maltose binding protein (MBP), ketoisovalerate decarboxylase (Kivd) and alcohol dehydrogenase (AdhP) were purified with high cleavage efficiency. The purified Kivd and AdhP remained high specific activities. This work demonstrated an effective and convenient protein purification method.

Microfluidic chip coupled with optical biosensors for simultaneous detection of multiple analytes: A review.

This article reviews the recent advances in microfluidic-chip integrated optical biosensors for simultaneous detection of multiple analytes. In particular, the principles and recent progress in different kinds of multiplex optical biosensors and their biological application were reviewed comprehensively. Sensors based on multiplexed detection have absolute advantages in analysis throughput than single assay. The microfluidic chip, a type of micro-total analysis system (µTAS), provides an ideal platform for integration of high-throughput biosensors. Compared with electronic biosensors, benefitted from the technical development in Micro-Electro-Mechanical System, there have been greater advances in the fabrication of optical sensors and microfluidic chip, and then promoting microfluidic-chip integrated optical biosensors for simultaneous detection of multiple analytes.

Simultaneous label-free screening of G-quadruplex active ligands from natural medicine via a microfluidic chip electrophoresis-based energy transfer multi-biosensor strategy.

Rapid screening of active compounds plays a crucial role in the research and application of complex natural medicines. Herein, a new method of simultaneous label-free multi-drug screening based on a selective aptamer-carboxyfluorescein/graphene oxide energy transfer optical sensor combined with microfluidic chip electrophoretic separation is reported. In this study, seven traditional Chinese medicinal monomers were chosen as targets for the screening of G-quadruplex ligands. The screening results of the G-quadruplex active ligands, including daidzein, berberine hydrochloride, jatrorrhizine hydrochloride, and fangchinoline, and non-active ligands, including geniposide and oxymatrine, were consistent with those reported in literature. Moreover, one new potential G4DNA active drug, jujuboside A, was identified. Molecular simulation of the interaction between G4DNA and drugs was also carried out using HyperChem and AutoDock to verify the results of the experimental screening. It further demonstrated the reliability of our strategy. This novel separation and concentration based multi-sensing strategy provides a simple, rapid, and sensitive tool for simultaneous multi-drug screening, which is very meaningful for drug screening and bio-interaction analysis.

α-Synuclein binds to cytoplasmic vesicles in U251 glioblastoma cells.

α-Synuclein is the major component of Lewy bodies, Lewy neurites, and glial cytoplasmic inclusions. It plays an important role in neurodegenerative diseases such as Parkinson's disease, multiple system atrophy, and other synucleinopathies. However, the pathogenesis and neurodegenerative effects of α-synuclein remain unknown. In this study, we established an α-synuclein and an α-synuclein-EGFP overexpressing U251 cell line. α-Synuclein overexpression increases oxidative stress and alters the cell surface and mitochondrial morphologies. We provide fluorescent-protein tagging, immunofluorescence and ultrastructural evidence showing that α-synuclein accumulations are associated with clusters of cytoplasmic vesicles and the diameter of these vesicles increases by H2O2 in a time- and dose-dependent manner.

Membrane electrospray ionization for direct ultrasensitive biomarker quantitation in biofluids using mass spectrometry.

The ability of rapid biomarker quantitation in raw biological samples would expand the application of mass spectrometry in clinical diagnosis. Up until now, the conventional chromatography-mass spectrometry method is time-consuming in both sample preparation and chromatography separation processes, while ambient ionization methods normally suffer from sensitivity. The membrane electrospray ionization (MESI) introduced in this study could not only achieve sensitive biomolecule quantitation, but also minimize the sample handling process. As a unique feature of MESI, both vertical and horizontal chemical separations could be achieved in real-time. With the capability of mass-selectively minimizing matrix effects from salts, small molecules, and macromolecules, ultrasensitive detection of cytochrome C (>500-fold sensitivity improvement) in raw urine samples was demonstrated in less than 20 min.

A newly discovered neurotoxin ADTIQ associated with hyperglycemia and Parkinson's disease.

BACKGROUND: Diabetes is associated with an increased risk of Parkinson's disease (PD). Number of studies have suggested that methylglyoxal (MGO) induced by diabetes is related to PD. However, very little is known about its molecular mechanism. On other hand, 1-acetyl-6, 7- dihydroxyl-1, 2, 3, 4- Tetrahydroisoquinoline(ADTIQ) is a dopamine (DA)-derived tetrahydroisoquinoline (TIQ), a novel endogenous neurotoxins, which was first discovered in frozen Parkinson's disease human brain tissue. While ADTIQ precursor methylglyoxal was also found in diabetic patients related to the glucose metabolism and diabetic patients. METHODS: LC-MS/MS, 1H NMR and infrared spectroscopy identified the structure of ADTIQ. The Annexin V-FITC/PI, MTT and western blot analysis were used to measure the neurotoxicity of ADTIQ. The levels of ADTIQ and methylglyoxal were detected by LC-MS/MS. RESULTS: Here we report the chemical synthesis of ADTIQ, demonstrate its biosynthesis in SH-SY5Y neuroblastoma cell line and investigate its role in the pathogenesis of PD. In addition, a significant increase in the level of ADTIQ was detected in the brains of transgenic mice expressing mutant forms (A53T or A30P) of α-synuclein. ADTIQ also reduced the cell viability and induced mitochondrial apoptosis in dopaminergic cells, suggesting that ADTIQ acts as an endogenous neurotoxin and potentially involved in the pathogenesis of PD. Methylglyoxal, a major byproduct of glucose metabolism and abnormalities in glucose metabolism could influence the levels of ADTIQ. Consistent with the hypothesis, increased levels of ADTIQ and methylglyoxal were detected in the striatum of diabetic rats and SH-SY5Y cells cultured in the presence of high glucose concentrations. CONCLUSIONS: Increased levels of ADTIQ could be related with Hyperglycemia and death of dopaminergic neurons. GENERAL SIGNIFICANCE: The increased levels of ADTIQ could be a reason of dopamine neuron dysfunction in diabetes. Therefore, ADTIQ may play a key role in increasing the risk for PD in patients with diabetes.

Methylglyoxal increases dopamine level and leads to oxidative stress in SH-SY5Y cells.

More and more studies have suggested that methylglyoxal (MGO) induced by type-2 diabetes is related to Parkinson's disease (PD). However, little is known about the molecular mechanism. In this study, we explored the MGO toxicity in neuroblastoma SH-SY5Y cells. Neurotoxicity of MGO was measured by mitochondrial membrane potential, malondialdehyde, and methylthiazoletetrazolium assays. The levels of dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC), and 1-methyl-4-phenyl-1,2,3,4-tetrahydroisoquinoline (salsolinol) were detected by liquid chromatography-mass spectrometry/mass spectrometry. The expressions of tyrosine hydroxylase (TH) and dopamine transporter (DAT) were detected by reverse transcriptase polymerase chain reaction and western blot analysis. The results showed that MGO induced an increase in TH and DAT expressions in SH-SY5Y neuroblastoma cells, while the levels of dopamine, DOPAC, and endogenous neurotoxin salsolinol also increased. Aminoguanidine (AG) is an inhibitor of MGO. It was found that AG could decrease the reactive oxygen species (ROS) level induced by MGO, but could not inhibit an increase of TH, DAT and dopamine. The increase of dopamine, DOPAC and salsolinol levels could lead to high ROS and mitochondrial damage. This study suggests that ROS caused by dopamine could contribute to the damage of dopaminergic neurons when MGO is increased during the course of diabetes.

Radioprotective effects of Dragon's blood and its extract against gamma irradiation in mouse bone marrow cells.

PURPOSE: The radioprotective effects of Dragon's blood (DB) and its extracts (DBE) were investigated using the chromosomal aberrant test, micronucleus and oxidative stress assay for anti-clastogenic and anti-oxidative activity. MATERIALS AND METHODS: Adult BALB/C mice were exposed to the whole body irradiation with 4 Gy (60)Co γ-rays. DB and DBE were administered orally once a day from 5 days prior to irradiation treatment to 1 day after irradiation. The mice were sacrificed on 24 h after irradiation. The cells of bone marrow were measured by counting different types of chromosomal aberrations and the frequency of micronuclei. Oxidative stress response was carried out by analysis of serum from blood. RESULTS: DB and DBE significantly decreased the number of bone marrow cells with chromosome aberrations after irradiation with respect to irradiated alone group. The administration of DB and DBE also significantly reduced the frequencies of micronucleated polychromatic erythrocytes (MPCE) and micronucleated normochromatic erythrocytes (MNCE). In addition, DB and DBE markedly increased the activity of antioxidant enzymes and the level of antioxidant molecular. Malondialdehyde (MDA) and nitric oxide (NO) levels in serum were significantly reduced by DB and DBE treatment. CONCLUSIONS: Our data suggested that DB and DBE have potential radioprotective properties in mouse bone marrow after (60)Co γ-ray exposure, which support their candidature as a potential radioprotective agent.

Microcystin-LR inhibited hippocampal long-term potential via regulation of the glycogen synthase kinase-3ß pathway.

We previously demonstrated that Cyanobacteria-derived microcystin-LR (MCLR) is able to induce cognitive dysfunction, but the mechanism is not understood. Long-term potential (LTP) in hippocampus is regarded as an important cellular mechanism of learning and memory. Here, the aim of this study was to evaluate the role of MCLR in LTP of hippocampal dentate gyrus (DG) by in vivo electrophysiological recording. We found that MCLR could suppress the induction of LTP in rat hippocampus, whereas simultaneous inhibition of glycogen synthase kinase-3ß (GSK-3ß) by LiCl or SB216763 attenuated the LTP impairments by MCLR. Furthermore, a decrease of the phosphorylated level at Ser9 of GSK-3ß was observed by western blotting after intracerebroventricular (ICV) injection of MCLR, indicating GSK-3ß was activated by MCLR. In addition, we showed that ICV administration of MCLR slightly stimulated activity of protein phosphatases (PPs) in the brain, which might activate GSK-3ß via dephosphorylation of Ser9 site. Taken together, these findings demonstrated that GSK-3ß plays a crucial role in regulating MCLR-induced cognitive deficit.

Increased levels of monoamine-derived potential neurotoxins in fetal rat brain exposed to ethanol.

Pregnant SD rats were exposed to ethanol (25 % (v/v) ethanol at 1.0, 2.0 or 4.0 g/kg body weight from GD8 to GD20) to assess whether ethanol-derived acetaldehyde could interact with endogenous monoamine to generate tetrahydroisoquinoline or tetrahydro-beta-carboline in the fetuses. The fetal brain concentration of acetaldehyde increased remarkably after ethanol administration (2.6 times, 5.3 times and 7.8 times as compared to saline control in 1.0, 2.0 and 4.0 g/kg ethanol-treated groups, respectively) detected by HPLC with 2,4-dinitrophenylhydrazine derivatization. Compared to control, ethanol exposure induced the formation of 1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (salsolinol, Sal), N-methyl-salsolinol (NMSal) and 1-methyl-6-hydroxy-1,2,3,4-tetrahydro-beta-carboline (6-OH-MTHBC) in fetal rat brains. Determined by HPLC with electrochemical detector, the levels of dopamine and 5-hydroxytryptamine in whole fetal brain were not remarkably altered by ethanol treatment, while the levels of homovanillic acid and 5-hydroxyindole acetic acid in high dose (4.0 g/kg) of ethanol-treated rats were significantly decreased compared to that in the control animals. 4.0 g/kg ethanol administration inhibited the activity of mitochondrial monoamine oxidase (51.3 % as compared to control) and reduced the activity of respiratory chain complex I (61.2 % as compared to control). These results suggested that ethanol-induced alteration of monoamine metabolism and the accumulation of dopamine-derived catechol isoquinolines and 5-hydroxytryptamine-derived tetrahydro-beta-carbolines may play roles in the developmental dysfuction of monoaminergic neuronal systems.

α-Synuclein increases U251 cells vulnerability to hydrogen peroxide by disrupting calcium homeostasis.

Multiple system atrophy (MSA) is a progressive neurodegenerative disease characterized by glial cytoplasmic inclusions containing insoluble α-synuclein. Since Ca(2+) plays an important role in cell degeneration, [Ca(2+)]( i ) in α-synuclein-overexpressed human glioma cells was analyzed by Fura-2 fluorometry. Overexpression of α-synuclein increased the basal level of [Ca(2+)]( i ), and a higher Ca(2+) response to hydrogen peroxide was further observed. The effect that α-synuclein overexpression caused U251 cells to be more vulnerable to hydrogen peroxide was eliminated by Ca(2+) chelator BAPTA-AM or transient receptor potential channels blocker SKF 96365 but not by L-type Ca(2+) channel blocker nimodipine. These findings suggest that the dysregulation of cellular Ca(2+) homeostasis caused by α-synuclein under oxidative stress may contribute to the glial cell death in MSA.

CAPIH: a Web interface for comparative analyses and visualization of host-HIV protein-protein interactions.

BACKGROUND: The Human Immunodeficiency Virus type one (HIV-1) is the major causing pathogen of the Acquired Immune Deficiency Syndrome (AIDS). A large number of HIV-1-related studies are based on three non-human model animals: chimpanzee, rhesus macaque, and mouse. However, the differences in host-HIV-1 interactions between human and these model organisms have remained unexplored. DESCRIPTION: Here we present CAPIH (Comparative Analysis of Protein Interactions for HIV-1), the first web-based interface to provide comparative information between human and the three model organisms in the context of host-HIV-1 protein interactions. CAPIH identifies genetic changes that occur in HIV-1-interacting host proteins. In a total of 1,370 orthologous protein sets, CAPIH identifies approximately 86,000 amino acid substitutions, approximately 21,000 insertions/deletions, and approximately 33,000 potential post-translational modifications that occur only in one of the four compared species. CAPIH also provides an interactive interface to display the host-HIV-1 protein interaction networks, the presence/absence of orthologous proteins in the model organisms in the networks, the genetic changes that occur in the protein nodes, and the functional domains and potential protein interaction hot sites that may be affected by the genetic changes. The CAPIH interface is freely accessible at http://bioinfo-dbb.nhri.org.tw/capih. CONCLUSION: CAPIH exemplifies that large divergences exist in disease-associated proteins between human and the model animals. Since all of the newly developed medications must be tested in model animals before entering clinical trials, it is advisable that comparative analyses be performed to ensure proper translations of animal-based studies. In the case of AIDS, the host-HIV-1 protein interactions apparently have differed to a great extent among the compared species. An integrated protein network comparison among the four species will probably shed new lights on AIDS studies.

Redox modulation of long-term potentiation in the hippocampus via regulation of the glycogen synthase kinase-3beta pathway.

Alzheimer disease (AD) is an age-related neurodegenerative disorder. Many observations indicate that impaired redox regulation is implicated in AD with synaptic failure. The aim of the current investigation was to characterize the role of redox-active agents on long-term potentiation (LTP) in the CA1 region of rat hippocampal slices and to elucidate the molecular sequence of events leading to these changes. The results presented here indicate that the membrane-permeable oxidizing agent chloramine-T (CH-T) inhibits the induction of LTP, whereas the membrane-permeable reducing agent dithiothreitol (DTT) enhances the induction of LTP. In contrast, neither the membrane-impermeable oxidizing agent 5,5'-dithio-bis-(2-nitrobenzoic acid) (DTNB) nor the membrane-impermeable reducing agent tris-(2-carboxyethyl) phosphine (TCEP) can affect the induction of LTP. The inhibition of LTP by CH-T can be restored by pretreatment with DTT but not with TCEP, whereas the enhancement of LTP by DTT can be reversed by pretreatment with CH-T but not with DTNB. We also provide evidence that the CH-T-evoked inhibition of LTP is mediated via activation of glycogen synthase kinase-3beta (GSK-3beta), whereas the DTT-evoked enhancement of LTP is mediated via inactivation of GSK-3beta. These findings will benefit the understanding of the redox contribution to the mechanisms underlying synaptic plasticity and AD pathogenesis.

Puerarin facilitates Ca(2+)-induced Ca(2+) release triggered by KCl-depolarization in primary cultured rat hippocampal neurons.

The effects of puerarin on behaviour and brain neuronal activity in animal studies have been described previously. However, molecule mechanisms underlying these effects were poorly understood. Here, we examined the regulation of puerarin on the Ca(2+) signals in primary rat hippocampal neurons using Fura-2 based calcium imaging techniques. Application of puerarin had no effect on the basal intracellular calcium concentration ([Ca(2+)](i)), but potentiated the KCl-evoked [Ca(2+)](i) transient in 87% of recorded neurons. Dantrolene or ruthenium red, the inhibitors of ryanodine receptors, completely blocked this potentiation induced by puerarin. Moreover, in Ca(2+)-free solution, pre-application of puerarin significantly augmented the elevation of [Ca(2+)](i) evoked by caffeine (3 mM), which is a specific agent to activate the ryanodine receptors. In contrast, nifedipine failed to prevent the potentiation induced by puerarin. Similarly, in the experiments of whole-cell patch-clamp recording, puerarin did not show any effect on calcium currents generated by depolarization pulses. These data demonstrated that the potentiation induced by puerarin was attributed to the facilitation of Ca(2+)-induced Ca(2+) release (CICR) via ryanodine receptors, rather than extracellular Ca(2+) influx. Using estrogen receptor antagonist ICI 182780 and tamoxifen, we further demonstrated that the potentiation induced by puerarin was mediated by the estrogen receptor. Furthermore, the membrane-permeant inhibitor of protein kinase A (PKA) H89 completely inhibited this potentiation. However, U-73122, the inhibitor of phospholipase C (PLC) had no effect, indicating that the cyclic AMP/PKA signaling pathway was involved in the activation of CICR by puerarin.

[Effects of electrical stimulation of the parafascicular nucleus on the neuronal activities of the subthalamic nucleus and the ventromedial nucleus in rats].

The present study was designed to investigate the function and mechanism of high-frequency stimulation (HFS) of the parafascicular nucleus (PF) used as a therapeutic approach for Parkinson's disease (PD). PD rat model was built by injecting 6-hydroxydopamine (6-OHDA) into the substartia nigra pars compacta of adult male Sprague-Dawley rats. Using the ethological methods, we examined the effect of electrical stimulation of PF on the apomorphine-induced rotational behavior in PD rats. Moreover, Electrophysiological recordings were made in rats to investigate the effects of electrical stimulation of PF on the neuronal activities of the subthalamic nucleus (STN) and the ventromedial nucleus (VM). Our results showed that one week after HFS (130 Hz, 0.4 mA, 5 s) of PF, there was significant improvement in apomorphine-induced rotational behavior in PD rats. HFS of PF caused an inhibition of the majority of neurons (84%) recorded in the STN in PD rats. The majority of cells recorded in the VM of the thalamus responded to the HFS with an increase in their unitary discharge activity (81%). These effects were in a frequency-dependent manner. Only stimulus frequencies above 50 Hz were effective. Furthermore, employing microelectrophoresis, we demonstrated that glutamatergic and GABAergic afferent nerve fibers converged on the same STN neurons. These results show that the HFS of PF induces a reduction of the excitatory glutamatergic output from the PF which in turn results in deactivation of STN neurons. The reduction in tonic inhibitory drive from the basal ganglia induces a disinhibition of activity in the VM, a motor thalamic nucleus. In conclusion, the results suggest that HFS of PF may produce a therapeutic effect in PD rats, which is mediated by the nuclei of PF, STN and VM.

Fly-DPI: database of protein interactomes for D. melanogaster in the approach of systems biology.

BACKGROUND: Proteins control and mediate many biological activities of cells by interacting with other protein partners. This work presents a statistical model to predict protein interaction networks of Drosophila melanogaster based on insight into domain interactions. RESULTS: Three high-throughput yeast two-hybrid experiments and the collection in FlyBase were used as our starting datasets. The co-occurrences of domains in these interactive events are converted into a probability score of domain-domain interaction. These scores are used to infer putative interaction among all available open reading frames (ORFs) of fruit fly. Additionally, the likelihood function is used to estimate all potential protein-protein interactions. All parameters are successfully iterated and MLE is obtained for each pair of domains. Additionally, the maximized likelihood reaches its converged criteria and maintains the probability stable. The hybrid model achieves a high specificity with a loss of sensitivity, suggesting that the model may possess major features of protein-protein interactions. Several putative interactions predicted by the proposed hybrid model are supported by literatures, while experimental data with a low probability score indicate an uncertain reliability and require further proof of interaction.Fly-DPI is the online database used to present this work. It is an integrated proteomics tool with comprehensive protein annotation information from major databases as well as an effective means of predicting protein-protein interactions. As a novel search strategy, the ping-pong search is a naïve path map between two chosen proteins based on pre-computed shortest paths. Adopting effective filtering strategies will facilitate researchers in depicting the bird's eye view of the network of interest. Fly-DPI can be accessed at http://flydpi.nhri.org.tw. CONCLUSION: This work provides two reference systems, statistical and biological, to evaluate the reliability of protein interaction. First, the hybrid model statistically estimates both experimental and predicted protein interaction relationships. Second, the biological information for filtering and annotation itself is a strong indicator for the reliability of protein-protein interaction. The space-temporal or stage-specific expression patterns of genes are also critical for identifying proteins involved in a particular situation.

POWER: PhylOgenetic WEb Repeater--an integrated and user-optimized framework for biomolecular phylogenetic analysis.

POWER, the PhylOgenetic WEb Repeater, is a web-based service designed to perform user-friendly pipeline phylogenetic analysis. POWER uses an open-source LAMP structure and infers genetic distances and phylogenetic relationships using well-established algorithms (ClustalW and PHYLIP). POWER incorporates a novel tree builder based on the GD library to generate a high-quality tree topology according to the calculated result. POWER accepts either raw sequences in FASTA format or user-uploaded alignment output files. Through a user-friendly web interface, users can sketch a tree effortlessly in multiple steps. After a tree has been generated, users can freely set and modify parameters, select tree building algorithms, refine sequence alignments or edit the tree topology. All the information related to input sequences and the processing history is logged and downloadable for the user's reference. Furthermore, iterative tree construction can be performed by adding sequences to, or removing them from, a previously submitted job. POWER is accessible at http://power.nhri.org.tw.