Open Access. Powered by Scholars. Published by Universities.®

Life Sciences Commons

Open Access. Powered by Scholars. Published by Universities.®

Articles 1 - 11 of 11

Full-Text Articles in Life Sciences

Mcnamara 201412 Nih Scap Innocentive Challenge Solution - T-Bow Rainbow T-Cells And Tumor Cells Spatial Multiplexing Gene Expression Reporter System – Plus Supplement Plus Posters - 20151027 - Please Download "75" Instead, George Mcnamara Oct 2015

Mcnamara 201412 Nih Scap Innocentive Challenge Solution - T-Bow Rainbow T-Cells And Tumor Cells Spatial Multiplexing Gene Expression Reporter System – Plus Supplement Plus Posters - 20151027 - Please Download "75" Instead, George Mcnamara

George McNamara

McNamara 201412 NIH SCAP InnoCentive Challenge Solution - T-Bow Rainbow T-cells and Tumor Cells Spatial Multiplexing Gene Expression Reporter System – plus supplement plus posters - 20151027.

///

Please download the current 20151027 (October 27, 2015) Tattletales and T-Bow update from

http://works.bepress.com/gmcnamara/75/

The bepress web site is not letting me replace the old pdf here at "65" with the additional 10 pages update.

///

The download is my/Cooper lab solution (submission) to the 2014 NIH Single Cell Analysis Program (SCAP) InnoCentive Challenge, "Follow That Cell". I submitted the Solution on 20141215Mon (with 20 minutes to spare). The Challenge web page …


Flatbed Scanner Report - Optical Density Dynamic Range, George Mcnamara Mar 2012

Flatbed Scanner Report - Optical Density Dynamic Range, George Mcnamara

George McNamara

George McNamara (now at University of Miami) report for Hua Yu and Richard Jove, City of Hope National Medical Center, on optical density dynamic range of several flatbed scanners.


Introduction To Nanoscopy Nano-Talk, George Mcnamara Feb 2012

Introduction To Nanoscopy Nano-Talk, George Mcnamara

George McNamara

T7-1 is the designation for the LMRG Nanoscopy session at ABRF in Orlando, FL, on March 20, 2012. The PDF file here is a draft of my presentation.

May not be very helpful since (1) would probably help to know what is in my head and each slide will [hopefully] prompt me to say, and (2) 10 minute talk so I am going to push the "next slide" button after saying very little.

__________________

Publisher statement:

The T7-1 Introduction to Nanoscopy Nano Talk is copyrighted (c) George McNamara, 2012. Except for (1) screenshots from research articles (which are copyrighted by …


Rogers Pmn Movie - Background Information, George Mcnamara Feb 2012

Rogers Pmn Movie - Background Information, George Mcnamara

George McNamara

Please see

http://mdc.custhelp.com/app/answers/detail/a_id/18689/~/metamatters-newsletters

for my series of MetaMorph MetaMatters articles in volume 2, numbers 3 through 6, on the Rogers PMN Panorama data set.

http://mdc.custhelp.com/app/answers/detail/a_id/18689/~/metamatters-newsletters

Brief summary (for more, see the Word doc)


Mcnamara 2011 Mpmicro - Multi-Probe Microscopy (10/31/2011), George Mcnamara Oct 2011

Mcnamara 2011 Mpmicro - Multi-Probe Microscopy (10/31/2011), George Mcnamara

George McNamara

Multi-Probe Microscopy is an ~1500 page Word document summarizing what I know and/or found interesting in light microscopy, fluorescence microscopy and digital image analysis, from 1995-2005. Very little has been updated since 2005.


Lack Of Depolarization-Induced Suppression Of Inhibition (Dsi) In Layer 2/3 Interneurons That Receive Cannabinoid-Sensitive Inhibitory Inputs, Fouad Lemtiri-Chlieh, Eric S. Levine Sep 2007

Lack Of Depolarization-Induced Suppression Of Inhibition (Dsi) In Layer 2/3 Interneurons That Receive Cannabinoid-Sensitive Inhibitory Inputs, Fouad Lemtiri-Chlieh, Eric S. Levine

fouad Lemtiri-Chlieh

In layer 2/3 of neocortex, brief trains of action potentials in pyramidal neurons (PNs) induce the mobilization of endogenous cannabinoids (eCBs), resulting in a depression of GABA release from the terminals of inhibitory interneurons (INs). This depolarization-induced suppression of inhibition (DSI) is mediated by activation of the type 1 cannabinoid receptor (CB1) on presynaptic terminals of a subset of INs. However, it is not clear whether CB1 receptors are also expressed at synapses between INs, and whether INs can release eCBs in response to depolarization. In the present studies, brain slices containing somatosensory cortex were prepared from 14- to 21-day-old …


Inhibition Of Astroglial Kir4.1 Channels By Selective Serotonin Reuptake Inhibitors, Y. Ohno, H. Hibino, Christoph Lossin, A. Inanobe, Y. Kurachi Jan 2007

Inhibition Of Astroglial Kir4.1 Channels By Selective Serotonin Reuptake Inhibitors, Y. Ohno, H. Hibino, Christoph Lossin, A. Inanobe, Y. Kurachi

Christoph Lossin, Ph.D.

The inwardly rectifying K+ (Kir) channel Kir4.1 is responsible for astroglial K+ buffering. We recently found that tricyclic antidepressants (TCAs) inhibit Kir4.1 channel currents, which suggests that astroglial Kir currents might be involved in the pharmacological action of antidepressants. We therefore further examined the effects of the currently most popular antidepressants, selective serotonin reuptake inhibitors (SSRIs), and other related agents on Kir4.1 channels heterologously expressed in HEK293T cells. The whole-cell patch clamp technique was used. Fluoxetine, the typical SSRI, inhibited Kir4.1 channel currents in a concentration-dependent manner with an IC50 value of 15.2 microM. The inhibitory effect of fluoxetine was …


Inhibition Of Astroglial Inwardly Rectifying Kir4.1 Channels By A Tricyclic Antidepressant, Nortriptyline., S. Su, Y. Ohno, Christoph Lossin, A. Inanobe, Y. Kurachi Jan 2007

Inhibition Of Astroglial Inwardly Rectifying Kir4.1 Channels By A Tricyclic Antidepressant, Nortriptyline., S. Su, Y. Ohno, Christoph Lossin, A. Inanobe, Y. Kurachi

Christoph Lossin, Ph.D.

The inwardly rectifying K(+) (Kir) channel Kir4.1 is responsible for astroglial K(+) buffering. We examined the effects of nortriptyline, a tricyclic antidepressant (TCA), on Kir4.1 channel currents heterologously expressed in HEK293T cells, using a whole-cell patch-clamp technique. Nortriptyline (3-300 microM) reversibly inhibited Kir4.1 currents in a concentration-dependent manner, whereas it marginally affected neuronal Kir2.1 currents. The inhibition of Kir4.1 channels by nortriptyline depended on the voltage difference from the K(+) equilibrium potential (E(K)), with greater potency at more positive potentials. Blocking kinetics of the drug could be described by first-order kinetics, where dissociation of the drug slowed down and association …


Non-Inactivating Voltage-Gated Sodium Channels In Severe Myoclonic Epilepsy Of Infancy, T. H. Rhodes, Christoph Lossin, C. Vanoye, Alfred L. George Jan 2004

Non-Inactivating Voltage-Gated Sodium Channels In Severe Myoclonic Epilepsy Of Infancy, T. H. Rhodes, Christoph Lossin, C. Vanoye, Alfred L. George

Christoph Lossin, Ph.D.

Mutations in SCN1A, the gene encoding the brain voltage-gated sodium channel alpha(1) subunit (Na(V)1.1), are associated with at least two forms of epilepsy, generalized epilepsy with febrile seizures plus and severe myoclonic epilepsy of infancy (SMEI). We examined the functional properties of five SMEI mutations by using whole-cell patch-clamp analysis of heterologously expressed recombinant human SCN1A. Two mutations (F902C and G1674R) rendered SCN1A channels nonfunctional, and a third allele (G1749E) exhibited minimal functional alterations. However, two mutations within or near the S4 segment of the fourth repeat domain (R1648C and F1661S) conferred significant impairments in fast inactivation, including persistent, noninactivating …


Presence Of A Cs-Resistant Transient Outward Current Which Distorts Ica Measurements In Guinea-Pig Single Ventricular Cells, Georges Christé, Brigitte Delachapelle, Fouad Lemtiri-Chlieh, Carlos Ojeda Nov 1989

Presence Of A Cs-Resistant Transient Outward Current Which Distorts Ica Measurements In Guinea-Pig Single Ventricular Cells, Georges Christé, Brigitte Delachapelle, Fouad Lemtiri-Chlieh, Carlos Ojeda

fouad Lemtiri-Chlieh

To correctlyr analyse the physical properties of ion channels and the actions of drugs upon them, it is important that the membrane conducts only the ionic species believed permeant. In guinea-pig ventricular cells it has been assumed that only ICaL flows in the potential range -50 to +60 mV in the presence of intra- and extracellular Cs (> 20 mM). We report here that this is not the case due to the presence of a Cs-insensitive, transient outward current.


Measurements Of Cytosolic Free Ca In Cultured Rat Neonate And Adult Guinea-Pig Ventricular Cardiac Myocytes, Jean-Claude Bernengo, Fouad Lemtiri-Chlieh, Carlos Ojeda, Nadine Pltonoff Nov 1989

Measurements Of Cytosolic Free Ca In Cultured Rat Neonate And Adult Guinea-Pig Ventricular Cardiac Myocytes, Jean-Claude Bernengo, Fouad Lemtiri-Chlieh, Carlos Ojeda, Nadine Pltonoff

fouad Lemtiri-Chlieh

Cytosolic free Ca was measured with Indo-1 (Grynkiewicz et al. 1985) as free acid (in guinea-pig cells) or as the ester (in rat neonate cells). Using image analysis we obtained concentration maps at 40 ms intervals at two wavelengths (Cannell et al. 1986). In rat neonate cells, at rest and during contraction, calcium was apparently non-uniformly distributed, in contrast to guinea-pig adult cells. Using a dual PM spectroscopic system adapted to an inverted microscope we found: (1) the conversion of Indo-AM to Indo- 1 in the cytosol is not complete (< 40% contribution to the total light); (2) rat neonate cells buffer Ca (at rest 130-170 nM) only for [Ca]. between 1 and 3 mM, whereas in adult guinea-pig cells the range extended to 10 mM; (3) during contraction [Ca]i rose from 200 nm to no more than 1 microM. Digitoxin increases basal and peak [Ca]i; (4) during spontaneous contractions, in guinea-pig cells, [Ca]i rises from 70 to 200 nm when [Ca]o = 0, and from 170 nm to about 1 microM when [Ca]o = 2 mM; (5) in voltage-clamp conditions the rise in [Ca]i does not exceed 2 microM and oscillations occur in the presence of forskolin. When loading with Indo-1, cells frequently cease to contract (Powell et al. 1988) and the variations in [Ca]i are then very small (about 200 nm at peak ICa). In both cases these values are small compared to the total charge crossing the membrane.