Docality.com Logo
 
Dr. James  Walsh  Md image

Dr. James Walsh Md

300 Community Dr
Manhasset NY 11030
516 624-4887
Medical School: New York Medical College - 1980
Accepts Medicare: Yes
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: No
License #: 152502
NPI: 1255337986
Taxonomy Codes:
207L00000X

Request Appointment Information

Awards & Recognitions

About Us

Practice Philosophy

Conditions

Dr. James Walsh is associated with these group practices

Procedure Pricing

HCPCS Code Description Average Price Average Price
Allowed By Medicare
HCPCS Code:00740 Description:Anesth upper gi visualize Average Price:$1,562.50 Average Price Allowed
By Medicare:
$170.58

Medical Malpractice Cases

None Found

Medical Board Sanctions

None Found

Referrals

NPI
Doctor Name
Specialty
Count
1144380205
Pulmonary Disease
85
1205806023
Infectious Disease
78
1952348310
Diagnostic Radiology
73
1720159114
Cardiovascular Disease (Cardiology)
53
1265466825
Diagnostic Radiology
49
1952391997
Gastroenterology
46
1801819354
Critical Care (Intensivists)
41
1851419717
Interventional Radiology
39
1275603318
Cardiovascular Disease (Cardiology)
29
1861599441
Interventional Radiology
26
*These referrals represent the top 10 that Dr. Walsh has made to other doctors

Publications

Improving the efficiency of electrochemical CO2 reduction using immobilized manganese complexes. - Faraday discussions
Immobilization of [Mn(bpy)(CO)3Br], () and [Mn(bpy((t)Bu)2)(CO)3Br] (, where (bpy((t)Bu)2) = 4,4'-di-tert-butyl-2,2'-bipyridine) in Nafion/multi-walled carbon nanotubes (MWCNT) on glassy carbon yielded highly active electrodes for the reduction of CO2 to CO in aqueous solutions at pH 7. Films incorporating have significantly improved selectivity towards CO2, with CO : H2 ∼ 1 at -1.4 V vs. SCE, exceeding that for the previously reported /MWCNT/Nafion electrode. Furthermore, we report the synthesis and subsequent electrochemical characterization of two new substituted Mn(i) bipyridine complexes, [Mn(bpy(COOH)2)(CO)3Br] () and [Mn(bpy(OH)2)(CO)3Br] () (where (bpy(COOH)2) = 4,4'-di-carboxy-2,2'-bipyridine and (bpy(OH)2) = 4,4'-di-hydroxy-2,2'-bipyridine). Both and were found to have some activity towards CO2 in acetonitrile solutions; however once immobilized in Nafion membranes CO2 reduction was found to not occur at significant levels.
Dealing with Danger in the CNS: The Response of the Immune System to Injury. - Neuron
Fighting pathogens and maintaining tissue homeostasis are prerequisites for survival. Both of these functions are upheld by the immune system, though the latter is often overlooked in the context of the CNS. The mere presence of immune cells in the CNS was long considered a hallmark of pathology, but this view has been recently challenged by studies demonstrating that immunological signaling can confer pivotal neuroprotective effects on the injured CNS. In this review, we describe the temporal sequence of immunological events that follow CNS injury. Beginning with immediate changes at the injury site, including death of neural cells and release of damage-associated molecular patterns (DAMPs), and progressing through innate and adaptive immune responses, we describe the cascade of inflammatory mediators and the implications of their post-injury effects. We conclude by proposing a revised interpretation of immune privilege in the brain, which takes beneficial neuro-immune communications into account.Copyright © 2015 Elsevier Inc. All rights reserved.
Esmirtazapine in non-elderly adult patients with primary insomnia: efficacy and safety from a 2-week randomized outpatient trial. - Sleep medicine
Esmirtazapine (Org 50081), a high-affinity antagonist at 5-HT2A and H1 receptors, was assessed for its hypnotic efficacy.In this double-blind, randomized study, non-elderly patients with primary insomnia (but otherwise healthy) were treated with esmirtazapine (1.5, 3.0, or 4.5 mg) or placebo for two weeks. The primary end point was patient-reported total sleep time (TST); other patient-reported end points included sleep latency (SL), wake time after sleep onset (WASO), number of awakenings, sleep quality, and satisfaction with sleep duration. Measures to assess the potential adverse effects of treatment included morning alertness, daytime function/napping, and rebound insomnia during a single-blind placebo run-out week after treatment ended. Adverse events (AEs) were also assessed.Overall, 526 patients were randomized and 463 (88%) completed treatment. All esmirtazapine doses significantly improved TST, SL, sleep quality, and satisfaction with sleep duration versus placebo. Relative to placebo, TST was increased by 30-40 min and SL decreased by ~12 min for all doses. The highest dose (4.5 mg) also significantly reduced WASO and number of awakenings. Across doses, AEs occurred in 25.5-32.8% of patients, compared with 20.7% with placebo. The most common AE was somnolence (~10% for esmirtazapine and 2% for placebo). The incidence of AEs leading to discontinuation was low (≤7%), and there were no serious drug-related AEs. Finally, there was no evidence of a rebound insomnia after discontinuation of esmirtazapine.Two weeks of treatment with esmirtazapine consistently and significantly improved patient-reported sleep parameters, and it was well tolerated in patients with primary insomnia.Copyright © 2015. Published by Elsevier B.V.
Molecular Interactions of the Min Protein System Reproduce Spatiotemporal Patterning in Growing and Dividing Escherichia coli Cells. - PloS one
Oscillations of the Min protein system are involved in the correct midcell placement of the divisome during Escherichia coli cell division. Based on molecular interactions of the Min system, we formulated a mathematical model that reproduces Min patterning during cell growth and division. Specifically, the increase in the residence time of MinD attached to the membrane as its own concentration increases, is accounted for by dimerisation of membrane-bound MinD and its interaction with MinE. Simulation of this system generates unparalleled correlation between the waveshape of experimental and theoretical MinD distributions, suggesting that the dominant interactions of the physical system have been successfully incorporated into the model. For cells where MinD is fully-labelled with GFP, the model reproduces the stationary localization of MinD-GFP for short cells, followed by oscillations from pole to pole in larger cells, and the transition to the symmetric distribution during cell filamentation. Cells containing a secondary, GFP-labelled MinD display a contrasting pattern. The model is able to account for these differences, including temporary midcell localization just prior to division, by increasing the rate constant controlling MinD ATPase and heterotetramer dissociation. For both experimental conditions, the model can explain how cell division results in an equal distribution of MinD and MinE in the two daughter cells, and accounts for the temperature dependence of the period of Min oscillations. Thus, we show that while other interactions may be present, they are not needed to reproduce the main characteristics of the Min system in vivo.
Discrete and polymeric cobalt organophosphates: isolation of a 3-D cobalt phosphate framework exhibiting selective CO2 capture. - Dalton transactions (Cambridge, England : 2003)
Structurally diverse mononuclear, dinuclear, and tetranuclear cobalt organophosphates and a three-dimensional framework based on a D4R cobalt phosphate are reported. The role of auxiliary ligands in determining the nuclearity of the phosphate clusters has further been established. Reaction of cobalt acetate tetrahydrate with 2,6-di-iso-propylphenylphosphate (dippH2) in methanol or DMSO in the presence of ancillary N-donor ligands leads to the formation of mononuclear octahedral cobalt phosphate [Co(dippH)2(py)4] (1), dinuclear octahedral cobalt phosphates [Co(dipp)(NN)(MeOH)2]2·2MeOH (NN = bpy 2; phen 3), tetrahedral cobalt phosphates [Co(dipp)(L)2]2·2(MeOH) (L = imz 4; dmpz 5) and symmetric and asymmetric tetranuclear tetrahedral cobalt phosphates [Co(dipp)(2-apy)]4 (6) and [Co4(dipp)4(2-apy)3(DMSO)]·(DMSO)·(H2O) (7), in nearly quantitative yields. The use of a linear N-donor ditopic linker, 3,6-di(pyridin-4-yl)-1,2,4,5-tetrazine (dptz), as the ancillary ligand leads to the formation of a robust three dimensional, four-fold interpenetrated network based on the D4R platform, {[Co(dipp)(dptz)0.5]4}n (8), under ambient conditions. The new compounds have been characterized by analytical, thermo-analytical and spectroscopic techniques. Further, the molecular structures of compounds 1-8 have been established using single crystal X-ray diffraction studies. Compound 1 is a mononuclear complex in which the dippH ligands occupy trans-positions around the octahedral cobalt ion. The core structure of compounds 2-5, a Co2P2O4 ring, resembles the S4R (single-4-ring) SBU of zeolites, whereas the Co4P4O12 inorganic core found in compounds 6 and 7 resembles the D4R (double-4-ring) SBU. Cobalt organophosphate framework 8 shows significant CO2 adsorption at 273 K (7.73 wt% at 1 bar and 18.21 wt% at 15.5 bar) with high selectivity to CO2 uptake over N2 and H2 at 273 K. Magnetic studies of these symmetric complexes indicate the presence of weak antiferromagnetic interactions between the metal ions via the phosphate bridging moiety.
The glia-derived alarmin IL-33 orchestrates the immune response and promotes recovery following CNS injury. - Neuron
Inflammation is a prominent feature of CNS injury that heavily influences neuronal survival, yet the signals that initiate and control it remain poorly understood. Here we identify the nuclear alarmin, interleukin (IL)-33, as an important regulator of the innate immune response after CNS injury. IL-33 is expressed widely throughout the healthy brain and is concentrated in white mater due to predominant expression in post-mitotic oligodendrocytes. IL-33 is released immediately after CNS injury from damaged oligodendrocytes, acting on local astrocytes and microglia to induce chemokines critical for monocyte recruitment. Mice lacking IL-33 have impaired recovery after CNS injury, which is associated with reduced myeloid cell infiltrates and decreased induction of M2 genes at the injury site. These results demonstrate a novel molecular mediator contributing to immune cell recruitment to the injured CNS and may lead to new therapeutic insights in CNS injury and neurodegenerative diseases.Copyright © 2015 Elsevier Inc. All rights reserved.
Interpretive bias, repressive coping, and trait anxiety. - Anxiety, stress, and coping
According to vigilance-avoidance theory, repressors have an avoidant interpretive bias, i.e., they interpret ambiguous self-relevant situations in a nonthreatening fashion. This study sought to demarcate the range of situations associated with avoidant interpretive bias in repressors.Four groups of participants, representing the four combinations of low- and high-trait anxiety and defensiveness, were identified. Those low in trait anxiety and high in defensiveness were categorized as repressors.Participants (N = 163) rated their likelihood of making both threatening and nonthreatening interpretations of 32 ambiguous scenarios over four domains: social, intellectual, physical, and health. Half the scenarios were self-relevant and half were other relevant. Brief measures of state anxiety were taken after each likelihood rating.Repressors displayed an avoidant interpretive bias for ambiguous threats in the social and intellectual domains but not the health or physical domains. This was due to repressors' low level of trait anxiety rather than their high defensiveness.Individuals high in trait anxiety are especially sensitive to situations involving social evaluation but not those characterized by danger to their health or physical well-being.
MHCII-independent CD4+ T cells protect injured CNS neurons via IL-4. - The Journal of clinical investigation
A body of experimental evidence suggests that T cells mediate neuroprotection following CNS injury; however, the antigen specificity of these T cells and how they mediate neuroprotection are unknown. Here, we have provided evidence that T cell-mediated neuroprotection after CNS injury can occur independently of major histocompatibility class II (MHCII) signaling to T cell receptors (TCRs). Using two murine models of CNS injury, we determined that damage-associated molecular mediators that originate from injured CNS tissue induce a population of neuroprotective, IL-4-producing T cells in an antigen-independent fashion. Compared with wild-type mice, IL-4-deficient animals had decreased functional recovery following CNS injury; however, transfer of CD4+ T cells from wild-type mice, but not from IL-4-deficient mice, enhanced neuronal survival. Using a culture-based system, we determined that T cell-derived IL-4 protects and induces recovery of injured neurons by activation of neuronal IL-4 receptors, which potentiated neurotrophin signaling via the AKT and MAPK pathways. Together, these findings demonstrate that damage-associated molecules from the injured CNS induce a neuroprotective T cell response that is independent of MHCII/TCR interactions and is MyD88 dependent. Moreover, our results indicate that IL-4 mediates neuroprotection and recovery of the injured CNS and suggest that strategies to enhance IL-4-producing CD4+ T cells have potential to attenuate axonal damage in the course of CNS injury in trauma, inflammation, or neurodegeneration.
CetZ tubulin-like proteins control archaeal cell shape. - Nature
Tubulin is a major component of the eukaryotic cytoskeleton, controlling cell shape, structure and dynamics, whereas its bacterial homologue FtsZ establishes the cytokinetic ring that constricts during cell division. How such different roles of tubulin and FtsZ evolved is unknown. Studying Archaea may provide clues as these organisms share characteristics with Eukarya and Bacteria. Here we report the structure and function of proteins from a distinct family related to tubulin and FtsZ, named CetZ, which co-exists with FtsZ in many archaea. CetZ X-ray crystal structures showed the FtsZ/tubulin superfamily fold, and one crystal form contained sheets of protofilaments, suggesting a structural role. However, inactivation of CetZ proteins in Haloferax volcanii did not affect cell division. Instead, CetZ1 was required for differentiation of the irregular plate-shaped cells into a rod-shaped cell type that was essential for normal swimming motility. CetZ1 formed dynamic cytoskeletal structures in vivo, relating to its capacity to remodel the cell envelope and direct rod formation. CetZ2 was also implicated in H. volcanii cell shape control. Our findings expand the known roles of the FtsZ/tubulin superfamily to include archaeal cell shape dynamics, suggesting that a cytoskeletal role might predate eukaryotic cell evolution, and they support the premise that a major function of the microbial rod shape is to facilitate swimming.
Suvorexant in Patients with Insomnia: Results from Two 3-Month Randomized Controlled Clinical Trials. - Biological psychiatry
Suvorexant is an orexin receptor antagonist for treatment of insomnia. We report results from two pivotal phase 3 trials.Two randomized, double-blind, placebo-controlled, parallel-group, 3-month trials in nonelderly (18-64 years) and elderly (≥65 years) patients with insomnia. Suvorexant doses of 40/30 mg (nonelderly/elderly) and 20/15 mg (nonelderly/elderly) were evaluated. The primary focus was 40/30 mg, with fewer patients randomized to 20/15 mg. There was an optional 3-month double-blind extension in trial 1. Each trial included a 1-week, randomized, double-blind run-out after double-blind treatment to assess withdrawal/rebound. Efficacy was assessed at week 1, month 1, and month 3 by patient-reported subjective total sleep time and time to sleep onset and in a subset of patients at night 1, month 1, and month 3 by polysomnography end points of wakefulness after persistent sleep onset and latency to onset of persistent sleep (LPS). One thousand twenty-one patients were randomized in trial 1 and 1019 patients in trial 2.Suvorexant 40/30 mg was superior to placebo on all subjective and polysomnography end points at night 1/week 1, month 1, and month 3 in both trials, except for LPS at month 3 in trial 2. Suvorexant 20/15 mg was superior to placebo on subjective total sleep time and wakefulness after persistent sleep onset at night 1/week 1, month 1, and month 3 in both trials and at most individual time points for subjective time to sleep onset and LPS in each trial. Both doses of suvorexant were generally well tolerated, with <5% of patients discontinuing due to adverse events over 3 months. The results did not suggest the emergence of marked rebound or withdrawal signs or symptoms when suvorexant was discontinued.Suvorexant improved sleep onset and maintenance over 3 months of nightly treatment and was generally safe and well tolerated.Copyright © 2014 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

Map & Directions

300 Community Dr Manhasset, NY 11030
View Directions In Google Maps

Nearby Doctors

300 Community Dr
Manhasset, NY 11030
516 623-3090
300 Community Dr Dept Of Anesthesia
Manhasset, NY 11030
516 624-4887
300 Community Dr Department Of Radiology
Manhasset, NY 11030
516 624-4797
Nsuh-Dept Of Pathology 300 Community Drive
Manhasset, NY 11030
516 624-4192
300 Community Dr
Manhasset, NY 11030
516 624-4221
Nsuh Dept Of Medicine Division Of Gastroenterology 300 Community Drive
Manhasset, NY 11030
516 624-4281
400 Community Dr
Manhasset, NY 11030
516 623-3260
300 Community Dr 9 Tower, Dept Of Neurology
Manhasset, NY 11030
516 624-4300
1129 Northern Blvd
Manhasset, NY 11030
516 656-6077