1,475 research outputs found
Analysis of Brain Imaging Data for the Detection of Early Age Autism Spectrum Disorder Using Transfer Learning Approaches for Internet of Things
In recent years, advanced magnetic resonance imaging (MRI) methods including functional magnetic resonance imaging (fMRI) and structural magnetic resonance imaging (sMRI) have indicated an increase in the prevalence of neuropsychiatric disorders such as autism spectrum disorder (ASD), effects one out of six children worldwide. Data driven techniques along with medical image analysis techniques, such as computer-assisted diagnosis (CAD), benefiting from deep learning. With the use of artificial intelligence (AI) and IoT-based intelligent approaches, it would be convenient to support autistic children to adopt the new atmospheres. In this paper, we classify and represent learning tasks of the most powerful deep learning network such as convolution neural network (CNN) and transfer learning algorithm on a combination of data from autism brain imaging data exchange (ABIDE I and ABIDE II) datasets. Due to their four-dimensional nature (three spatial dimensions and one temporal dimension), the resting state-fMRI (rs-fMRI) data can be used to develop diagnostic biomarkers for brain dysfunction. ABIDE is a collaboration of global scientists, where ABIDE-I and ABIDE-II consists of 1112 rs-fMRI datasets from 573 typical control (TC) and 539 autism individuals, and 1114 rs-fMRI from 521 autism and 593 typical control individuals respectively, which were collected from 17 different sites. Our proposed optimized version of CNN achieved 81.56% accuracy. This outperforms prior conventional approaches presented only on the ABIDE I datasets
Comments on "Human dominant disease genes are enriched in paralogs originating from whole genome duplication"
OGEE v2: an update of the online gene essentiality database with special focus on differentially essential genes in human cancer cell lines
OGEE is an Online GEne Essentiality database. To enhance our understanding of the essentiality of genes, in OGEE we collected experimentally tested essential and non-essential genes, as well as associated gene properties known to contribute to gene essentiality. We focus on large-scale experiments, and complement our data with text-mining results. We organized tested genes into data sets according to their sources, and tagged those with variable essentiality statuses across data sets as conditionally essential genes, intending to highlight the complex interplay between gene functions and environments/experimental perturbations. Developments since the last public release include increased numbers of species and gene essentiality data sets, inclusion of non-coding essential sequences and genes with intermediate essentiality statuses. In addition, we included 16 essentiality data sets from cancer cell lines, corresponding to 9 human cancers; with OGEE, users can easily explore the shared and differentially essential genes within and between cancer types. These genes, especially those derived from cell lines that are similar to tumor samples, could reveal the oncogenic drivers, paralogous gene expression pattern and chromosomal structure of the corresponding cancer types, and can be further screened to identify targets for cancer therapy and/or new drug development. OGEE is freely available at http://ogee.medgenius.info
Surgical excision promotes tumor growth and metastasis by promoting expression of MMP-9 and VEGF in a breast cancer model
Surgery is still the main curative therapeutic modality for breast cancer. Although surgery often results in the successful removal of the primary tumor, its process could increase the risk of metastases of residual cancer cells. Understanding of the connection between breast cancer metastasis and surgical wound will lead to the establishment of a proper treatment strategy for postoperative cancer patient. Aim: To study the influence of surgical procedure on the metastasis of primary breast cancer. Methods: We established MDA-MB-435 human breast cancer xenograft model. Levels of Pro-matrix metalloproteinase 9 (Pro-MMP-9) and vascular endothelial growth factor (VEGF) in host serum and tumors were tested at different time points with ELISA and zymography and correlated to tumor growth and postoperative metastasis. Results: Our study demonstrated surgical wound had promoting effect on tumor growth and pulmonary metastasis of human breast cells, if tumor cells remain in bodies. This effect might be related to the postoperative interaction of cancer and host cells, which resulted in expression of Pro-MMP-9. Surgical process could also increase the VEGF expression in tumor tissues. Conclusions: Surgical wound-produced host Pro-MMP-9 and tumor cell VEGF might be important mediators leading to metastasis of residual breast cancer after surgery.Π₯ΠΈΡΡΡΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ΅ Π»Π΅ΡΠ΅Π½ΠΈΠ΅ Π΄ΠΎ ΡΠΈΡ
ΠΏΠΎΡ ΠΎΡΡΠ°Π΅ΡΡΡ Π³Π»Π°Π²Π½ΡΠΌ ΡΠ΅ΡΠ°ΠΏΠ΅Π²ΡΠΈΡΠ΅ΡΠΊΠΈΠΌ ΠΏΠΎΠ΄Ρ
ΠΎΠ΄ΠΎΠΌ ΠΏΡΠΈ Π»Π΅ΡΠ΅Π½ΠΈΠΈ Π±ΠΎΠ»ΡΠ½ΡΡ
ΡΠ°ΠΊΠΎΠΌ ΠΌΠΎΠ»ΠΎΡΠ½ΠΎΠΉ
ΠΆΠ΅Π»Π΅Π·Ρ. Π₯ΠΎΡΡ Ρ
ΠΈΡΡΡΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ΅ ΡΠ΄Π°Π»Π΅Π½ΠΈΠ΅ ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ Π² Π±ΠΎΠ»ΡΡΠΈΠ½ΡΡΠ²Π΅ ΡΠ»ΡΡΠ°Π΅Π² Π΄ΠΎΡΡΠ°ΡΠΎΡΠ½ΠΎ ΡΡΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎ, Π² ΡΠΎ ΠΆΠ΅ Π²ΡΠ΅ΠΌΡ ΠΎΠ½ΠΎ ΠΌΠΎΠΆΠ΅Ρ
ΡΠ²Π΅Π»ΠΈΡΠΈΡΡ ΡΠΈΡΠΊ ΠΌΠ΅ΡΠ°ΡΡΠ°Π·ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΎΡΡΠ°ΡΠΎΡΠ½ΡΡ
ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ. ΠΠΎΠ½ΠΈΠΌΠ°Π½ΠΈΠ΅ ΡΠ²ΡΠ·ΠΈ ΠΌΠ΅ΠΆΠ΄Ρ ΠΌΠ΅ΡΠ°ΡΡΠ°Π·ΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ΠΌ ΠΏΡΠΈ ΡΠ°ΠΊΠ΅
ΠΌΠΎΠ»ΠΎΡΠ½ΠΎΠΉ ΠΆΠ΅Π»Π΅Π·Ρ ΠΈ ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΎΠ½Π½ΠΎΠΉ ΡΠ°Π½ΠΎΠΉ ΠΏΠΎΠ·Π²ΠΎΠ»ΠΈΡ Π²ΡΠ±ΡΠ°ΡΡ Π½Π°ΠΈΠ»ΡΡΡΡΡ ΡΡΡΠ°ΡΠ΅Π³ΠΈΡ ΠΏΠΎΡΡΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΎΠ½Π½ΠΎΠ³ΠΎ Π»Π΅ΡΠ΅Π½ΠΈΡ. Π¦Π΅Π»Ρ:
ΠΎΠΏΡΠ΅Π΄Π΅Π»ΠΈΡΡ Π²Π»ΠΈΡΠ½ΠΈΠ΅ Ρ
ΠΈΡΡΡΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π²ΠΌΠ΅ΡΠ°ΡΠ΅Π»ΡΡΡΠ²Π° Π½Π° ΠΌΠ΅ΡΠ°ΡΡΠ°Π·ΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ. ΠΠ΅ΡΠΎΠ΄Ρ: Π±ΡΠ»Π° ΡΠΎΠ·Π΄Π°Π½Π° ΠΌΠΎΠ΄Π΅Π»Ρ ΡΠ°ΠΊΠ°
ΠΌΠΎΠ»ΠΎΡΠ½ΠΎΠΉ ΠΆΠ΅Π»Π΅Π·Ρ ΡΠ΅Π»ΠΎΠ²Π΅ΠΊΠ° Π² Π²ΠΈΠ΄Π΅ ΠΊΡΠ΅Π½ΠΎΡΡΠ°Π½ΡΠΏΠ»Π°Π½ΡΠ°ΡΠ° MDA-MB-435. Π£ΡΠΎΠ²Π΅Π½Ρ Pro-ΠΌΠ°ΡΡΠΈΡΠ½ΠΎΠΉ ΠΌΠ΅ΡΠ°Π»Π»ΠΎΠΏΡΠΎΡΠ΅ΠΈΠ½Π°Π·Ρ 9
(Pro-MMP-9) ΠΈ ΡΠ°ΠΊΡΠΎΡΠ° ΡΠΎΡΡΠ° ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΡ ΡΠΎΡΡΠ΄ΠΎΠ² (VEGF) Π² ΡΡΠ²ΠΎΡΠΎΡΠΊΠ΅ ΡΠ΅ΡΠΈΠΏΠΈΠ΅Π½ΡΠ° ΠΈ ΠΎΠΏΡΡ
ΠΎΠ»ΡΡ
ΠΎΡΠ΅Π½ΠΈΠ²Π°Π»ΠΈΡΡ Π² ΡΠ°Π·Π½ΡΠ΅
Π²ΡΠ΅ΠΌΠ΅Π½Π½ΡΠ΅ ΠΏΡΠΎΠΌΠ΅ΠΆΡΡΠΊΠΈ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ELISA ΠΈ Π·ΠΈΠΌΠΎΠ³ΡΠ°ΡΠΈΠΈ. ΠΡΠΈ ΡΡΠΎΠΌ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ»ΠΈ Π½Π°Π»ΠΈΡΠΈΠ΅ ΠΊΠΎΡΠ΅Π»Π»ΡΡΠΈΠΈ ΠΌΠ΅ΠΆΠ΄Ρ ΡΡΠΈΠΌΠΈ ΠΏΠΎΠΊΠ°Π·Π°- ΠΈ Π·ΠΈΠΌΠΎΠ³ΡΠ°ΡΠΈΠΈ. ΠΡΠΈ ΡΡΠΎΠΌ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ»ΠΈ Π½Π°Π»ΠΈΡΠΈΠ΅ ΠΊΠΎΡΠ΅Π»Π»ΡΡΠΈΠΈ ΠΌΠ΅ΠΆΠ΄Ρ ΡΡΠΈΠΌΠΈ ΠΏΠΎΠΊΠ°Π·Π° ΠΈ Π·ΠΈΠΌΠΎΠ³ΡΠ°ΡΠΈΠΈ. ΠΡΠΈ ΡΡΠΎΠΌ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ»ΠΈ Π½Π°Π»ΠΈΡΠΈΠ΅ ΠΊΠΎΡΠ΅Π»Π»ΡΡΠΈΠΈ ΠΌΠ΅ΠΆΠ΄Ρ ΡΡΠΈΠΌΠΈ ΠΏΠΎΠΊΠ°Π·Π°ΡΠ΅Π»ΡΠΌΠΈ,
ΡΠΎΡΡΠΎΠΌ ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ ΠΈ ΠΏΠΎΡΡΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΎΠ½Π½ΡΠΌΠΈ ΠΌΠ΅ΡΠ°ΡΡΠ°Π·Π°ΠΌΠΈ. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ: Π±ΡΠ»ΠΎ ΠΏΠΎΠΊΠ°Π·Π°Π½ΠΎ, ΡΡΠΎ ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΎΠ½Π½Π°Ρ ΡΠ°Π½Π° ΡΠΏΠΎΡΠΎΠ±ΡΡΠ²ΡΠ΅Ρ
ΡΠΎΡΡΡ ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ ΠΌΠΎΠ»ΠΎΡΠ½ΠΎΠΉ ΠΆΠ΅Π»Π΅Π·Ρ ΠΈ Π΅Π΅ ΠΌΠ΅ΡΠ°ΡΡΠ°Π·ΠΈΡΠΎΠ²Π°Π½ΠΈΡ Π² Π»Π΅Π³ΠΊΠΈΠ΅ Π² ΡΠ»ΡΡΠ°Π΅, ΠΊΠΎΠ³Π΄Π° ΠΏΡΠΈ ΡΠ΄Π°Π»Π΅Π½ΠΈΠΈ ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ Π² ΡΠ°Π½Π΅
ΠΎΡΡΠ°ΡΡΡΡ ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΡΠ΅ ΠΊΠ»Π΅ΡΠΊΠΈ. ΠΡΠΎ ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ ΡΠ²ΡΠ·Π°Π½ΠΎ Ρ ΠΏΠΎΡΡΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΎΠ½Π½ΡΠΌ Π²Π·Π°ΠΈΠΌΠΎΠ΄Π΅ΠΉΡΡΠ²ΠΈΠ΅ΠΌ ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΡΡ
ΠΈ ΠΎΠΊΡΡΠΆΠ°ΡΡΠΈΡ
ΠΈΡ
Π½ΠΎΡΠΌΠ°Π»ΡΠ½ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ, ΠΊΠΎΡΠΎΡΠΎΠ΅ ΠΏΡΠΈΠ²ΠΎΠ΄ΠΈΡ ΠΊ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ Pro-MMP-9. Π£Π΄Π°Π»Π΅Π½ΠΈΠ΅ ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ ΠΌΠΎΠΆΠ΅Ρ ΡΠ°ΠΊΠΆΠ΅ ΡΠΏΠΎΡΠΎΠ±ΡΡΠ²ΠΎΠ²Π°ΡΡ
ΡΠ²Π΅Π»ΠΈΡΠ΅Π½ΠΈΡ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ VEGF ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΡΠΌΠΈ ΠΊΠ»Π΅ΡΠΊΠ°ΠΌΠΈ. ΠΡΠ²ΠΎΠ΄Ρ: Pro-MMP-9, ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡΡΠ΅ΠΌΡΠΉ Π½ΠΎΡΠΌΠ°Π»ΡΠ½ΡΠΌΠΈ ΠΊΠ»Π΅ΡΠΊΠ°ΠΌΠΈ,
ΠΎΠΊΡΡΠΆΠ°ΡΡΠΈΠΌΠΈ ΠΏΠΎΡΡΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΎΠ½Π½ΡΡ ΡΠ°Π½Ρ, Π° ΡΠ°ΠΊΠΆΠ΅ VEGF, ΠΏΡΠΎΠ΄ΡΡΠΈΡΡΠ΅ΠΌΡΠΉ ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΡΠΌΠΈ ΠΊΠ»Π΅ΡΠΊΠ°ΠΌΠΈ, ΠΌΠΎΠ³ΡΡ Π±ΡΡΡ Π²Π°ΠΆΠ½ΡΠΌΠΈ
ΠΌΠ΅Π΄ΠΈΠ°ΡΠΎΡΠ°ΠΌΠΈ ΠΌΠ΅ΡΠ°ΡΡΠ°Π·ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΎΡΡΠ°ΡΠΎΡΠ½ΡΡ
ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ ΠΏΠΎΡΠ»Π΅ Ρ
ΠΈΡΡΡΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π²ΠΌΠ΅ΡΠ°ΡΠ΅Π»ΡΡΡΠ²Π°
Influence of the detector's temperature on the quantum Zeno effect
In this paper we study the quantum Zeno effect using the irreversible model
of the measurement. The detector is modeled as a harmonic oscillator
interacting with the environment. The oscillator is subjected to the force,
proportional to the energy of the measured system. We use the Lindblad-type
master equation to model the interaction with the environment. The influence of
the detector's temperature on the quantum Zeno effect is obtained. It is shown
that the quantum Zeno effect becomes stronger (the jump probability decreases)
when the detector's temperature increases
Recommended from our members
Unbiased, optimal, and in-betweens: the trade-off in discrete finite impulse response filtering
In this survey, the authors examine the trade-off between the unbiased, optimal, and in-between solutions in finite impulse response (FIR) filtering. Specifically, they refer to linear discrete real-time invariant state-space models with zero mean noise sources having arbitrary covariances (not obligatorily delta shaped) and distributions (not obligatorily Gaussian). They systematically analyse the following batch filtering algorithms: unbiased FIR (UFIR) subject to the unbiasedness condition, optimal FIR (OFIR) which minimises the mean square error (MSE), OFIR with embedded unbiasedness (EU) which minimises the MSE subject to the unbiasedness constraint, and optimal UFIR (OUFIR) which minimises the MSE in the UFIR estimate. Based on extensive investigations of the polynomial and harmonic models, the authors show that the OFIR-EU and OUFIR filters have higher immunity against errors in the noise statistics and better robustness against temporary model uncertainties than the OFIR and Kalman filters
Ξ±-Mg primary phase formation and dendritic morphology transition in solidification of a Mg-Nd-Gd-Zn-Zr casting alloy
Effect of Hyperglycemia on Gene Expression during Early Organogenesis in Mice
BACKGROUND: Cardiovascular and neural malformations are common sequels of diabetic pregnancies, but the underlying molecular mechanisms remain unknown. We hypothesized that maternal hyperglycemia would affect the embryos most shortly after the glucose-sensitive time window at embryonic day (ED) 7.5 in mice. METHODS: Mice were made diabetic with streptozotocin, treated with slow-release insulin implants and mated. Pregnancy aggravated hyperglycemia. Gene expression profiles were determined in ED8.5 and ED9.5 embryos from diabetic and control mice using Serial Analysis of Gene Expression and deep sequencing. RESULTS: Maternal hyperglycemia induced differential regulation of 1,024 and 2,148 unique functional genes on ED8.5 and ED9.5, respectively, mostly in downward direction. Pathway analysis showed that ED8.5 embryos suffered mainly from impaired cell proliferation, and ED9.5 embryos from impaired cytoskeletal remodeling and oxidative phosphorylation (all P β€ E-5). A query of the Mouse Genome Database showed that 20-25% of the differentially expressed genes were caused by cardiovascular and/or neural malformations, if deficient. Despite high glucose levels in embryos with maternal hyperglycemia and a ~150-fold higher rate of ATP production from glycolysis than from oxidative phosphorylation on ED9.5, ATP production from both glycolysis and oxidative phosphorylation was reduced to ~70% of controls, implying a shortage of energy production in hyperglycemic embryos. CONCLUSION: Maternal hyperglycemia suppressed cell proliferation during gastrulation and cytoskeletal remodeling during early organogenesis. 20-25% of the genes that were differentially regulated by hyperglycemia were associated with relevant congenital malformations. Unexpectedly, maternal hyperglycemia also endangered the energy supply of the embryo by suppressing its glycolytic capacity
Long-distance quantum communication with "polarization" maximally entangled states
We propose a scheme for long-distance quantum communication where the
elementary entanglement is generated through two-photon interference and
quantum swapping is performed through one-photon interference. Local
"polarization" maximally entangled states of atomic ensembles are generated by
absorbing a single photon from on-demand single-photon sources. This scheme is
robust against phase fluctuations in the quantum channels, moreover speeds up
long-distance high-fidelity entanglement generation rate.Comment: 5 pages 5 figure
Maternal diabetes causes developmental delay and death in early-somite mouse embryos
Maternal diabetes causes congenital malformations and delays embryonic growth in the offspring. We investigated effects of maternal diabetes on mouse embryos during gastrulation and early organogenesis (ED7.5-11.5). Female mice were made diabetic with streptozotocin, treated with controlled-release insulin implants, and mated. Maternal blood glucose concentrations increased up to embryonic day (ED) 8.5. Maternal hyperglycemia induced severe growth retardation (approx.1 day) in 53% of the embryos on ED8.5, death in most of these embryos on ED9.5, and the termination of pregnancy on ED10.5 in litters with >20% dead embryos. Due to this selection, developmental delays and reduction in litter size were no longer observed thereafter in diabetic pregnancies. Male and female embryos were equally sensitive. High-throughput mRNA sequencing and pathway analysis of differentially expressed genes showed that retarded embryos failed to mount the adaptive suppression of gene expression that characterized non-retarded embryos (cell proliferation, cytoskeletal remodeling, oxidative phosphorylation). We conclude that failure of perigastrulation embryos of diabetic mothers to grow and survive is associated with their failure to shut down pathways that are strongly down-regulated in otherwise similar non-retarded embryos. Embryos that survive the early and generalized adverse effect of maternal diabetes, therefore, appear the subset in which malformations become manifest
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