Dimitrios Motakis

McGill University

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Michael A. Parniak

University of Pittsburgh

Yudong Quan

Chinese Academy of Agricultural Sciences

Stephanie Ma

New York University

Chen Lee

Beihang University

Marcin Czerwiński

Polish Academy of Sciences

Mark A. Wainberg

McGill University

Michael T. Flavin

New York Eye and Ear Infirmary

Robert W. Buckheit

ImQuest BioSciences (United States)

Ze‐Qi Xu

SynChem (United States)

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McGill University

Jewish General Hospital

McGill University Health Centre

Université de Montréal

Fundación Juan March

Southern Research Institute

University of Pittsburgh

Candy’s Place

National Institutes of Health

Magee-Womens Research Institute

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Sensitivity and Resistance to (+)-Calanolide a of Wild-Type and Mutated Forms of HIV-1 Reverse Transcriptase

Antiviral Therapy (1999)

Yudong Quan Dimitrios Motakis Robert W. Buckheit Ze‐Qi Xu Michael T. Flavin

We have tested both wild-type and drug-resistant mutated, recombinant human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) molecules for sensitivity to each of two non-nucleoside RT inhibitors (NNRTI), (+)-calanolide A and nevirapine, in primer extension assays. We found that RT containing either the V106A or Y181C substitutions, associated with NNRTI resistance, displayed approximately 90-fold resistance to nevirapine but remained fully sensitive to (+)-calanolide A and that the Y181C mutation marginally enhanced susceptibility to the latter drug. In contrast, the Y188H substitution in RT resulted in about 30-fold resistance to (+)-calanolide A in these assays but did not result in diminished sensitivity to nevirapine. Tissue culture results indicated that the combination of (+)-calanolide A and nevirapine possessed an additive to weakly synergistic effect in blocking replication of HIV-1 in tissue culture. These results suggest that (+)-calanolide A and nevirapine might have rationale as a combination therapy for HIV disease.

Nevirapine

Reverse-transcriptase inhibitor

Primer (cosmetics)

Resistance mutation

Wild type

Cross-resistance

10.1177/135965359900400403

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Economic Analysis of Open Approach Versus Conventional Methods of Zygoma Fracture Repair

Canadian Journal of Plastic Surgery (2008)

Marcin Czerwiński Stephanie Ma Dimitrios Motakis Chen Lee

As resource allocations in health care are being increasingly guided by cost containment issues, surgical professionals must consider the costs associated with various procedures. The present study identifies the financial costs attributed to the two principal treatment options available for zygoma fractures: the Gillie's method and open reduction and internal fixation (ORIF).Patients were included if they sustained an isolated zygoma fracture and were treated within 10 days of injury using either ORIF or the Gillie's method. Those who suffered concomitant injuries or required orbital floor exploration and repair were excluded. The end point, which consisted of the total cost required to bring a patient to preinjury facial appearance and function, incorporated the cost of primary treatment and that of any secondary procedures required to correct unfavourable outcomes.In total, 45 patients were included: 25 were treated with Gillie's method and 20 were treated with ORIF. The cost associated with the primary treatment of zygoma fractures was found to be higher for ORIF than Gillie's method, amounting to $1,811 and $715, respectively. However, when taking into account potential repair of unsatisfactory results, the final sum totalled $1,930 and $3,725, respectively. This difference was statistically significant.To the authors' knowledge, this is the first study to objectively examine the cost of the Gillie's method and ORIF in the repair of zygoma fractures. Although the initial cost of ORIF is higher, the final cost of the Gillie's method is greater. Thus, surgeons should not allow higher initial costs to deter them from using more extensive and accurate techniques.

10.1177/229255030801600308

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Citations (6)

A Tight-Binding Mode of Inhibition Is Essential for Anti-Human Immunodeficiency Virus Type 1 Virucidal Activity of Nonnucleoside Reverse Transcriptase Inhibitors

Antimicrobial Agents and Chemotherapy (2002)

Dimitrios Motakis Michael A. Parniak

ABSTRACT It was previously found that certain nonnucleoside reverse transcriptase inhibitors (NNRTI) possess virucidal activity against human immunodeficiency virus type 1 (HIV-1), and it was suggested that the tight-binding mode of inhibition of reverse transcriptase might be important for this virucidal activity (Borkow et al., J. Virol. 71:3023-3030, 1997). To test this, we compared six different NNRTI, including three tight-binding NNRTI, namely UC781, efavirenz (EFV) (Sustiva), and 5-chloro-3-phenylsulfonylindole-2-carboxamide (CSIC), and three rapid-equilibrium NNRTI, delavirdine (DLV) (Rescriptor), nevirapine (NVP) (Viramune), and UC84, in a variety of virucidal tests. Incubation of isolated HIV-1 virions with UC781, EFV, or CSIC rapidly inactivated the virus, whereas DLV, NVP, and UC84 were ineffective in this respect. Exposure of H9+ cells chronically infected by HIV-1 to the tight-binding NNRTI abolished the infectivity of nascent virus subsequently produced by these cells following removal of extracellular drug, thereby preventing cell-to-cell virus transmission in the absence of exogenous drug. In contrast, cell-to-cell transmission of HIV was blocked by DLV, NVP, and UC84 only when the drug remained in the extracellular medium. Pretreatment of uninfected lymphocytoid cells with UC781, EFV, or CSIC, but not DLV, NVP, or UC84, protected these cells from subsequent HIV-1 infection in the absence of extracellular drug. The protective effect was dependent on both the dose of NNRTI and the viral load. The overall virucidal efficacy of the tight-binding NNRTI tested was CSIC > UC781 ≃ EFV. We conclude that the tight-binding mode of inhibition is an essential characteristic for virucidal NNRTI and that antiviral potency is an insufficient predictor for virucidal utility of NNRTI.

Reverse-transcriptase inhibitor

Efavirenz

Nevirapine

Infectivity

10.1128/aac.46.6.1851-1856.2002

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Citations (63)