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Article: Multi-modulated frequency domain high density diffuse optical tomography.

Perkins, Guy A / Eggebrecht, Adam T / Dehghani, Hamid

2022 Volume 13, Issue 10, Page(s) 5275–5294

Abstract: Frequency domain (FD) high density diffuse optical tomography (HD-DOT) utilising varying or combined modulation frequencies (mFD) has shown to theoretically improve the imaging accuracy as compared to conventional continuous wave (CW) measurements. Using ...

Abstract	Frequency domain (FD) high density diffuse optical tomography (HD-DOT) utilising varying or combined modulation frequencies (mFD) has shown to theoretically improve the imaging accuracy as compared to conventional continuous wave (CW) measurements. Using intensity and phase data from a solid inhomogeneous phantom (NEUROPT) with three insertable rods containing different contrast anomalies, at modulation frequencies of 78 MHz, 141 MHz and 203 MHz, HD-DOT is applied and quantitatively evaluated, showing that mFD outperforms FD and CW for both absolute (iterative) and temporal (linear) tomographic imaging. The localization error (LOCA), full width half maximum (FWHM) and effective resolution (ERES) were evaluated. Across all rods, the LOCA of mFD was 61.3% better than FD and 106.1% better than CW. For FWHM, CW was 6.0% better than FD and mFD and for ERES, mFD was 1.20% better than FD and 9.83% better than CW. Using mFD data is shown to minimize the effect of inherently noisier FD phase data whilst maximising its strengths through improved contrast.
Language	English
Publishing date	2022-09-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	2572216-5
ISSN	2156-7085
ISSN	2156-7085
DOI	10.1364/BOE.467614
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Article: An Emerging Model for Cancer Development from a Tumor Microenvironment Perspective in Mice and Humans.

Yamaguchi, Ryuji / Perkins, Guy

Advances in experimental medicine and biology

2020 Volume 1225, Page(s) 19–29

Abstract: In the past, cancer development was studied in terms of genetic mutations acquired in cancer cells at each stage of the development. We present an emerging model for cancer development in which the tumor microenvironment (TME) plays an integral part. In ... ...

Abstract	In the past, cancer development was studied in terms of genetic mutations acquired in cancer cells at each stage of the development. We present an emerging model for cancer development in which the tumor microenvironment (TME) plays an integral part. In this model, the tumor development is initiated by a slowly growing nearly homogeneous colony of cancer cells that can evade detection by the cell's innate mechanism of immunity such as natural killer (NK) cells (first stage; colonization). Subsequently, the colony develops into a tumor filled with lymphocytes and stromal cells, releasing pro-inflammatory cytokines, growth factors, and chemokines (second stage; lymphocyte infiltration). Cancer progression proceeds to a well-vesiculated silent tumor releasing no inflammatory signal, being nearly devoid of lymphocytes (third stage; silenced). Eventually some cancer cells within a tumor undertake epithelial-to-mesenchymal transition (EMT), which leads to cancer metastasis (fourth stage; EMT). If a circulating metastasized cancer cell finds a niche in a new tissue and evades detection by NK cells, it can establish a new colony in which very few stromal cells are present (fifth stage; metastasis), which is much like a colony at the first stage of development. At every stage, cancer cells influence their own TME, and in turn, the TME influences the cancer cells contained within, either by direct interaction between cancer cells and stromal cells or through exchange of cytokines. In this article, we examine clinical findings and animal experiments pertaining to this paradigm-shifting model and consider if, indeed, some aspects of cancer development are governed solely by the TME.
MeSH term(s)	Animals ; Carcinogenesis/immunology ; Carcinogenesis/pathology ; Epithelial-Mesenchymal Transition ; Humans ; Killer Cells, Natural/immunology ; Neoplasms/immunology ; Neoplasms/pathology ; Neoplastic Cells, Circulating/immunology ; Neoplastic Cells, Circulating/pathology ; Stromal Cells/immunology ; Stromal Cells/pathology ; Tumor Microenvironment
Language	English
Publishing date	2020-02-06
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-3-030-35727-6_2
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Article ; Online: Quantitative evaluation of frequency domain measurements in high density diffuse optical tomography.

Perkins, Guy A / Eggebrecht, Adam T / Dehghani, Hamid

Journal of biomedical optics

2021 Volume 26, Issue 5

Abstract: Significance: High density diffuse optical tomography (HD-DOT) as applied in functional near-infrared spectroscopy (fNIRS) is largely limited to continuous wave (CW) data. Using a single modulation frequency, frequency domain (FD) HD-DOT has recently ... ...

Abstract	Significance: High density diffuse optical tomography (HD-DOT) as applied in functional near-infrared spectroscopy (fNIRS) is largely limited to continuous wave (CW) data. Using a single modulation frequency, frequency domain (FD) HD-DOT has recently demonstrated better localization of focal activation as compared to CW data. We show that combining CW and FD measurements and multiple modulation frequencies increases imaging performance in fNIRS. Aim: We evaluate the benefits of multiple modulation frequencies, combining different frequencies as well as CW data in fNIRS HD-DOT. Approach: A layered model was used, with activation occurring within a cortex layer. CW and FD measurements were simulated at 78, 141, and 203 MHz with and without noise. The localization error, full width half maximum, and effective resolution were evaluated. Results: Across the average of the three metrics, at 141 MHz, FD performed 8.4% better than CW, and the combination of CW and FD was 21.7% better than CW. FD measurements at 203 MHz performed 5% better than 78 MHz. Moreover, the three combined modulation frequencies of FD and CW performed up to 3.92% better than 141 MHz alone. Conclusions: We show that combining CW and FD measurements offers better performance than FD alone, with higher modulation frequencies increasing accuracy. Combining CW and FD measurements at multiple modulation frequencies yields the best overall performance.
MeSH term(s)	Spectroscopy, Near-Infrared ; Tomography, Optical
Language	English
Publishing date	2021-05-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1309154-2
ISSN	1560-2281 ; 1083-3668
ISSN (online)	1560-2281
ISSN	1083-3668
DOI	10.1117/1.JBO.26.5.056001
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Article ; Online: Structure versus function: Are new conformations of pannexin 1 yet to be resolved?

Mim, Carsten / Perkins, Guy / Dahl, Gerhard

The Journal of general physiology

2021 Volume 153, Issue 5

Abstract: Pannexin 1 (Panx1) plays a decisive role in multiple physiological and pathological settings, including oxygen delivery to tissues, mucociliary clearance in airways, sepsis, neuropathic pain, and epilepsy. It is widely accepted that Panx1 exerts its role ...

Abstract	Pannexin 1 (Panx1) plays a decisive role in multiple physiological and pathological settings, including oxygen delivery to tissues, mucociliary clearance in airways, sepsis, neuropathic pain, and epilepsy. It is widely accepted that Panx1 exerts its role in the context of purinergic signaling by providing a transmembrane pathway for ATP. However, under certain conditions, Panx1 can also act as a highly selective membrane channel for chloride ions without ATP permeability. A recent flurry of publications has provided structural information about the Panx1 channel. However, while these structures are consistent with a chloride selective channel, none show a conformation with strong support for the ATP release function of Panx1. In this Viewpoint, we critically assess the existing evidence for the function and structure of the Panx1 channel and conclude that the structure corresponding to the ATP permeation pathway is yet to be determined. We also list a set of additional topics needing attention and propose ways to attain the large-pore, ATP-permeable conformation of the Panx1 channel.
MeSH term(s)	Adenosine Triphosphate ; Connexins/metabolism ; Ion Channels/metabolism ; Nerve Tissue Proteins/metabolism ; Signal Transduction
Chemical Substances	Connexins ; Ion Channels ; Nerve Tissue Proteins ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2021-04-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3118-5
ISSN	1540-7748 ; 0022-1295
ISSN (online)	1540-7748
ISSN	0022-1295
DOI	10.1085/jgp.202012754
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Article ; Online: Enhanced mitochondrial buffering prevents Ca

Cheng, Hang / Perkins, Guy A / Ju, Saeyeon / Kim, Keunyoung / Ellisman, Mark H / Pamenter, Matthew E

The Journal of physiology

2023

Abstract: Deleterious ... ...

Abstract	Deleterious Ca
Language	English
Publishing date	2023-09-05
Publishing country	England
Document type	Journal Article
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/JP285002
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Article ; Online: The use of miniSOG in the localization of mitochondrial proteins.

Perkins, Guy A

Methods in enzymology

2014 Volume 547, Page(s) 165–179

Abstract: In this chapter, we provide details along with considerations and future directions for the use of miniSOG (for mini Singlet Oxygen Generator), a versatile label for correlated light and electron microscopy of genetically tagged proteins in cells, ... ...

Abstract	In this chapter, we provide details along with considerations and future directions for the use of miniSOG (for mini Singlet Oxygen Generator), a versatile label for correlated light and electron microscopy of genetically tagged proteins in cells, tissues, and organisms. This new visualizable genetic tag improves the ability of biologists to locate specific proteins at nanoscale resolution and to see these tagged proteins in the environment of structural landmarks that we are used to navigating by, such as mitochondrial membranes and compartments. miniSOG provides high-quality ultrastructural preservation and permits three-dimensional protein localization via electron tomography or serial section block-face scanning electron microscopy. miniSOG is now doing for electron microscopy what the family of green fluorescent protein did for fluorescence microscopy.
MeSH term(s)	Animals ; Calcium Channels/analysis ; Calcium Channels/genetics ; Calcium Channels/metabolism ; Cells, Cultured ; Electron Microscope Tomography/methods ; Light ; Microscopy, Electron/methods ; Microscopy, Electron, Scanning/methods ; Microtomy/methods ; Mitochondrial Proteins/analysis ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Oxidation-Reduction ; Phototropins/genetics ; Phototropins/metabolism ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism ; Rodentia ; Singlet Oxygen/metabolism ; Transfection/methods
Chemical Substances	Calcium Channels ; Mitochondrial Proteins ; Phototropins ; Recombinant Proteins ; mitochondrial calcium uniporter ; Singlet Oxygen (17778-80-2)
Language	English
Publishing date	2014
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1557-7988 ; 0076-6879
ISSN (online)	1557-7988
ISSN	0076-6879
DOI	10.1016/B978-0-12-801415-8.00010-2
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Article ; Online: Animal models for studying tumor microenvironment (TME) and resistance to lymphocytic infiltration.

Yamaguchi, Ryuji / Perkins, Guy

Cancer biology & therapy

2018 Volume 19, Issue 9, Page(s) 745–754

Abstract: In cancer immunotherapy, cytotoxic T or NK cells need to engage cancer cells to initiate the killing. However, in clinical studies and in mouse models, some solid tumors are found with no lymphocytes. It is likely that these tumors will be resistant to ... ...

Abstract	In cancer immunotherapy, cytotoxic T or NK cells need to engage cancer cells to initiate the killing. However, in clinical studies and in mouse models, some solid tumors are found with no lymphocytes. It is likely that these tumors will be resistant to all sorts of immunotherapies. Thus, restoring lymphocytic infiltration will be vital to the success of immunotherapies on solid tumors. In order to understand the complex interaction between cancer cells and stromal cells, we propose to establish animal models for studying the tumor microenvironment and to develop and test therapies to restore lymphocytic infiltration of tumors Without lymphocytes infiltrating tumors, all immunotherapies on solid tumors become ineffective.
MeSH term(s)	Animals ; Animals, Genetically Modified ; Biomarkers ; Disease Models, Animal ; Gene Expression Profiling ; Humans ; Immunotherapy ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism ; Killer Cells, Natural/pathology ; Lymphocytes, Tumor-Infiltrating/immunology ; Lymphocytes, Tumor-Infiltrating/pathology ; Mice ; Neoplasms/etiology ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/therapy ; T-Lymphocytes, Cytotoxic/immunology ; T-Lymphocytes, Cytotoxic/metabolism ; Tumor Microenvironment/immunology ; Xenograft Model Antitumor Assays
Chemical Substances	Biomarkers
Language	English
Publishing date	2018-05-16
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2146305-0
ISSN	1555-8576 ; 1538-4047
ISSN (online)	1555-8576
ISSN	1538-4047
DOI	10.1080/15384047.2018.1470722
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Article ; Online: Role of A-Kinase Anchoring Protein 1 in Retinal Ganglion Cells: Neurodegeneration and Neuroprotection.

Bastola, Tonking / Perkins, Guy A / Kim, Keun-Young / Choi, Seunghwan / Kwon, Jin-Woo / Shen, Ziyao / Strack, Stefan / Ju, Won-Kyu

Cells

2023 Volume 12, Issue 11

Abstract: A-Kinase anchoring protein 1 (AKAP1) is a multifunctional mitochondrial scaffold protein that regulates mitochondrial dynamics, bioenergetics, and calcium homeostasis by anchoring several proteins, including protein kinase A, to the outer mitochondrial ... ...

Abstract	A-Kinase anchoring protein 1 (AKAP1) is a multifunctional mitochondrial scaffold protein that regulates mitochondrial dynamics, bioenergetics, and calcium homeostasis by anchoring several proteins, including protein kinase A, to the outer mitochondrial membrane. Glaucoma is a complex, multifactorial disease characterized by a slow and progressive degeneration of the optic nerve and retinal ganglion cells (RGCs), ultimately resulting in vision loss. Impairment of the mitochondrial network and function is linked to glaucomatous neurodegeneration. Loss of AKAP1 induces dynamin-related protein 1 dephosphorylation-mediated mitochondrial fragmentation and loss of RGCs. Elevated intraocular pressure triggers a significant reduction in AKAP1 protein expression in the glaucomatous retina. Amplification of AKAP1 expression protects RGCs from oxidative stress. Hence, modulation of AKAP1 could be considered a potential therapeutic target for neuroprotective intervention in glaucoma and other mitochondria-associated optic neuropathies. This review covers the current research on the role of AKAP1 in the maintenance of mitochondrial dynamics, bioenergetics, and mitophagy in RGCs and provides a scientific basis to identify and develop new therapeutic strategies that could protect RGCs and their axons in glaucoma.
MeSH term(s)	Humans ; Retinal Ganglion Cells/metabolism ; A Kinase Anchor Proteins/metabolism ; Neuroprotection ; Glaucoma/metabolism ; Retina/metabolism
Chemical Substances	A Kinase Anchor Proteins
Language	English
Publishing date	2023-06-03
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12111539
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Article ; Online: Three-Dimensional Ultrastructure of the Normal Rod Photoreceptor Synapse and Degenerative Changes Induced by Retinal Detachment.

Torten, Gil / Fisher, Steven K / Linberg, Kenneth A / Luna, Gabriel / Perkins, Guy / Ellisman, Mark H / Williams, David S

The Journal of neuroscience : the official journal of the Society for Neuroscience

2023 Volume 43, Issue 30, Page(s) 5468–5482

Abstract: The rod photoreceptor synapse is the first synapse of dim-light vision and one of the most complex in the mammalian CNS. The components of its unique structure, a presynaptic ribbon and a single synaptic invagination enclosing several postsynaptic ... ...

Abstract	The rod photoreceptor synapse is the first synapse of dim-light vision and one of the most complex in the mammalian CNS. The components of its unique structure, a presynaptic ribbon and a single synaptic invagination enclosing several postsynaptic processes, have been identified, but disagreements about their organization remain. Here, we have used EM tomography to generate high-resolution images of 3-D volumes of the rod synapse from the female domestic cat. We have resolved the synaptic ribbon as a single structure, with a single arciform density, indicating the presence of one long site of transmitter release. The organization of the postsynaptic processes, which has been difficult to resolve with past methods, appears as a tetrad arrangement of two horizontal cell and two rod bipolar cell processes. Retinal detachment severely disrupts this organization. After 7 d, EM tomography reveals withdrawal of rod bipolar dendrites from most spherules; fragmentation of synaptic ribbons, which lose their tight association with the presynaptic membrane; and loss of the highly branched telodendria of the horizontal cell axon terminals. After detachment, the hilus, the opening through which postsynaptic processes enter the invagination, enlarges, exposing the normally sequestered environment within the invagination to the extracellular space of the outer plexiform layer. Our use of EM tomography provides the most accurate description to date of the complex rod synapse and details changes it undergoes during outer segment degeneration. These changes would be expected to disrupt the flow of information in the rod pathway.
MeSH term(s)	Female ; Animals ; Cats ; Retinal Detachment ; Microscopy, Electron ; Synapses/metabolism ; Retina/ultrastructure ; Retinal Bipolar Cells ; Retinal Rod Photoreceptor Cells/ultrastructure ; Mammals
Language	English
Publishing date	2023-07-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.2267-22.2023
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Article: Activating soluble adenylyl cyclase protects mitochondria, rescues retinal ganglion cells, and ameliorates visual dysfunction caused by oxidative stress.

Bastola, Tonking / Perkins, Guy A / Huu, Viet Anh Nguyen / Ju, Saeyeon / Kim, Keun-Young / Shen, Ziyao / Skowronska-Krawczyk, Dorota / Weinreb, Robert N / Ju, Won-Kyu

bioRxiv : the preprint server for biology

2024

Abstract: Oxidative stress is a key factor causing mitochondrial dysfunction and retinal ganglion cell (RGC) death in glaucomatous neurodegeneration. The cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signaling pathway is involved in mitochondrial ... ...

Abstract	Oxidative stress is a key factor causing mitochondrial dysfunction and retinal ganglion cell (RGC) death in glaucomatous neurodegeneration. The cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signaling pathway is involved in mitochondrial protection, promoting RGC survival. Soluble adenylyl cyclase (sAC) is one of the key regulators of the cAMP/PKA signaling pathway. However, the precise molecular mechanisms underlying the sAC-mediated signaling pathway and mitochondrial protection in RGCs that counter oxidative stress are not well characterized. Here, we demonstrate that sAC plays a critical role in protecting RGC mitochondria from oxidative stress. Using mouse models of oxidative stress, we found that activating sAC protected RGCs, blocked AMP-activated protein kinase activation, inhibited glial activation, and improved visual function. Moreover, we found that this is the result of preserving mitochondrial dynamics (fusion and fission), promoting mitochondrial bioenergetics and biogenesis, and preventing metabolic stress and apoptotic cell death in a paraquat oxidative stress model. Notably, sAC activation ameliorated mitochondrial dysfunction in RGCs by enhancing mitochondrial biogenesis, preserving mitochondrial structure, and increasing ATP production in oxidatively stressed RGCs. These findings suggest that activating sAC enhances the mitochondrial structure and function in RGCs to counter oxidative stress, consequently promoting RGC protection. We propose that modulation of the sAC-mediated signaling pathway has therapeutic potential acting on RGC mitochondria for treating glaucoma and other retinal diseases.
Language	English
Publishing date	2024-03-04
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.04.583371
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