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Dive into the research topics where Nighat N. Kahn is active.

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Featured researches published by Nighat N. Kahn.


Life Sciences | 1998

Insulin-induced expression of prostacyclin receptors on platelets is mediated through ADP-ribosylation of Giα protein

Nighat N. Kahn

The binding of insulin in physiological amounts to human blood platelets, which increases adenylate cyclase-linked prostacyclin receptor numbers on the cell surface, was found to be directly related to the ADP-ribosylation of the Gi alpha. Conversely, resuspension of the insulin-treated platelets in the hormone-free medium decreased both the prostaglandin receptor numbers and ADP-ribosylation of Gi alpha. Furthermore, incubation of platelets with pertussis toxin or its A-protomer, which ADP-ribosylates Gi alpha, also stimulated the binding of the prostanoid. These results suggest that the increase of prostacyclin receptor numbers in platelets is mediated through the ADP-ribosylation of Gi alpha.


Journal of Spinal Cord Medicine | 2010

Lower-Extremity Functional Electrical Stimulation Decreases Platelet Aggregation and Blood Coagulation in Persons With Chronic Spinal Cord Injury: A Pilot Study

Nighat N. Kahn; Susan P. Feldman; William A. Bauman

Abstract Background: Individuals with spinal cord injury (SCI) develop premature cardiovascular disease. Regular exercise reduces the incidence and symptoms of cardiovascular disease in able-bodied individuals; these salutary effects of exercise have not been documented in persons with SCI. Objective: To evaluate the effects of functional electrical stimulation leg cycle ergometry (FES-LCE) exercise training on platelet aggregation and blood coagulation in persons with SCI. Participants: Subjects (n = 14) with stable chronic (>1 year) paraplegia (T1-T10) or tetraplegia (C4-C8). Methods: Blood samples were collected before and after the first and eighth sessions (2 sessions per week for 4 weeks) of FES exercise. Results: Platelet aggregation was inhibited by 20% after the first session and by 40% (P < 0.001) after the eighth session. Thrombin activity was unchanged after the first session (10.7±0.85 s to 10.43±0.56 s) and decreased after the eighth session (12.5±1.98 s to 11.1±1.7 s; P < 0.0003). Antithrombin III activity increased after the first (103.8%±8.9% to 110%±6.9%; P < 0.0008) and eighth sessions (107.8%±12.1 % to 120.4%±13.1 %; P < 0.0001). Cyclic adenosine monophosphate increased after the first (9.9%±2.5% to 15.8%±3%; P < 0.001) and eighth sessions (17.8%±4.2% to 36.5%±7.6%; P < 0.0001). After the eighth session, factors V and X increased significantly (88%±27% to 103%±23%, P < 0.0001; 100%±40% to 105%±7%, P < 0.01, respectively); factors VII and VIII and fibrinogen did not change significantly. A significant reduction in platelet activation/aggregation was demonstrated in response to FES-LCE. The decrease in thrombin level was caused by the simultaneous increase in antithrombin activity. Conclusion: These findings provide new insight into the potential protective effects of FES-LCE against the risk of cardiovascular disease.


Journal of Spinal Cord Medicine | 2005

Appearance of a novel prostacyclin receptor antibody and duration of spinal cord injury.

Nighat N. Kahn; William A. Bauman; Asru K. Sinha

Abstract Background: Cardiovascular disease (CVD) appears to be accelerated in individuals with chronic spinal cord injury (SCI). Previously, we have identified a novel circulating antibody (lgG) in persons with SCI that specifically blocks the high-affinity prostacyclin (PGI) receptors on the platelet surface without affecting the low-affinity PGI 2 receptors. Objective: In this study, the relationship between the time course after SCI to the development of lgG to the high-affinity PGI 2 receptor was determined. Methods: Blood samples were collected 1, 3, 5, 10, and > 1 0 (15 ±4) years after SCI (n = 36). Plasma samples (50 11g) were analyzed by polyacrylamide gel electrophoresis (PAGE)followed by ensitometry. Results: The optical density (OD) of the lgG (molecular weight 47,000) at 1 year afterSCI was significantly higher than control (1 .65 ±0.08 vs 1.33 ±0.04; P < 0.01 ). Thisanti-receptor lgG appears to increase for 5 years and then plateau. At 5 years, 6-10 years,and > 10 years of injury, the OD was 1.83± 0.09, 1.83 ±0.1 0, and 1.87 ±0.08, respectively. With an increase in this specific lgG, there was a concomitant decrease in the binding of prostacyclin to its high-affinity receptors on SCIplatelets, (non-SCI vs 1, 3, and5years after injury; n1 = 1 72 ±25 vs 153 ±15, 1 07 ±25, and 40 ±4 sites/platelet, respectively; P < 0.001 ), with no significant change inreceptor affinity. Conclusions: The level of the high-affinity PGI2-receptor antibody determined in individuals with SCI was associated with the duration and not with the level of injury. Plateletsfrom subjects with SCI had a reduction in numbers of high-affinity receptors.


Platelets | 2003

Circulating heavy chain IgG, a pathological mediator for coronary artery disease, recognizes platelet surface receptors of both prostacyclin and insulin

Nighat N. Kahn; William A. Bauman; Asru K. Sinha

Although an increased incidence of premature cardiovascular disease has been determined to be the major cause of mortality in subjects with chronic spinal cord injury the identity of the pathophysiological mediators of cardiovascular disease in spinal cord injury remains obscure. Because both insulin and prostacyclin could be important in the prevention of thrombosis, the status of insulin-induced nitric oxide production and the prostacyclin high-affinity receptor interaction in platelets in subjects with spinal cord injury was studied. It was established that the insulin-induced nitric oxide synthesis in platelets from spinal cord-injured subjects was markedly impaired (0.053-0.058, P=0.37-0.44) compared to (0.062-0.53 μM/108 platelets, P<0.001) due to the presence of a free heavy chain IgG (Mr 47 kDa) in the circulation of subjects with spinal cord injury. This IgG not only blocked insulin receptor binding sites (without affecting dissociation constant of the hormone binding, Kd1= 2 × 10−9 M) for the synthesis of nitric oxide but also blocked the prostacyclin receptor interaction in normal platelets. Since the presence of circulating heavy chain of IgG could block the antithrombotic effect of both insulin and prostacyclin, the free heavy chain of the IgG molecule was thought to be one of the pathological mediators for the increased incidence of cardiovascular disease in individuals with spinal cord injury. The cross-reactivity of the free heavy chain with two different receptors antigens was thought to be related to the presence of several regions of homology in the amino acid sequence in the insulin and prostacyclin receptor molecules.


Journal of Breath Research | 2015

Biomarkers of inflammation in persons with chronic tetraplegia

Miroslav Radulovic; William A. Bauman; Jill M. Wecht; Michael F. LaFountaine; Nighat N. Kahn; Joshua C. Hobson; Kamaldeep Singh; Christopher Renzi; Christina Yen; Gregory J. Schilero

In addition to lung volume restriction, individuals with chronic tetraplegia exhibit reduced airway caliber and bronchodilator responsiveness similar to persons with asthma. In asthma, airflow obstruction is closely linked to airway inflammation. Conversely, little is known regarding the airway inflammatory response in tetraplegia. To compare levels of biomarkers of inflammation in exhaled breath condensate (EBC) and serum in subjects with chronic tetraplegia, mild asthma, and able-bodied controls.Prospective, observational pilot study. Thirty-four subjects participated: tetraplegia (n = 12), asthma (n = 12), controls (n = 10). Biomarkers in EBC [8-isoprostane (8-IP), leukotriene B4 (LT-B4), prostaglandin E2 (PG-E2), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6)] and serum (8-IP, LT-B4, TNF-α, IL-6) were determined using commercially available EIA kits (Cayman Chemical Company, Ann Arbor, MI). Separate, one-way ANOVA with Bonferronis post-hoc analyses were performed to determine group differences in demographic and dependent variables [EBC and serum biomarkers, fractional exhaled nitric oxide (FeNO), pulmonary function parameters, and specific airway conductance (sGaw)]. The tetraplegia group had significantly elevated 8-IP levels in EBC compared to the asthma (68 ± 38 versus 21 ± 13 pg ml(-1); p < 0.001) and control groups (22 ± 13 pg ml(-1); p < 0.01), respectively. FeNO levels were significantly elevated in the asthma compared to the control group (26 ± 18 versus 11 ± 4 ppb; p < 0.05), and trended higher than levels in the tetraplegia group (15 ± 6; p = 0.08). Levels of serum biomarkers did not differ significantly among groups. Through analysis of EBC, levels of 8-IP were significantly elevated compared to levels found in individuals with mild asthma and healthy controls. Further studies are needed to extend upon these preliminary findings that suggest the presence of airway inflammation in subjects with chronic tetraplegia, and how this relates to pulmonary dysfunction in this population.


Blood Coagulation & Fibrinolysis | 2015

Estriol-induced fibrinolysis due to the activation of plasminogen to plasmin by nitric oxide synthesis in platelets.

Pradipta Jana; Smarajit Maiti; Nighat N. Kahn; Asru K. Sinha

Estriol, an oestrogen, at 0.6 nmol/l was reported to inhibit ADP-induced platelet aggregation through nitric oxide synthesis. As nitric oxide has been reported to cause fibrinolysis due to the activation of plasminogen to plasmin, the role of estriol as a fibrinolytic agent was investigated. Also, the mechanism of estriol-induced nitric oxide synthesis in anucleated platelets was investigated. The estriol-induced lysis of platelet-rich plasma (PRP) clot was determined by photography of the clot lysis and by the assay of fibrin degradation products in the lysate and was obtained by SDS-PAGE. Nitric oxide was determined by methemoglobin method. The platelet membrane protein was isolated from the platelets by using Triton X-100 (0.05% v/v). The binding of estriol to the protein was determined by Scatchard plot by using an ELISA for estriol. Estriol at 0.6 nmol/l was found to lyse the clotted PRP due to fibrinolysis that produced fibrin degradation products in the lysate. The amino acid analysis of the platelet membrane protein, which resembles with nitric oxide synthase (NOS) activity, was activated nearly 10-fold over the control in the presence of estriol and was identified to be a human serum albumin precursor (Mr. 69 kDa) that binds to estriol with Kd1 of 6.0 × 10−9 mol/l and 39 ± 2 molecules of estriol bound the NOS molecule. The estriol-induced nitric oxide is capable of inducing fibrinolysis of the clotted PRP. The binding of estriol to platelet membrane NOS activated the enzyme in the absence of DNA in the platelet.


American Journal of Hematology | 2006

Effects of oxandrolone, an anabolic steroid, on hemostasis.

Nighat N. Kahn; Asru K. Sinha; Ann M. Spungen; William A. Bauman


Proceedings of the National Academy of Sciences of the United States of America | 1997

Demonstration of a novel circulating anti-prostacyclin receptor antibody

Nighat N. Kahn; William A. Bauman; Asru K. Sinha


Archive | 2005

Compositions and Methods for Modulating Insulin-Activated Nitric Oxide Synthase

Nighat N. Kahn; Asru K. Sinha


Archive | 2004

Nitric oxide inducing agents

Nighat N. Kahn; Asru K. Sinha

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Asru K. Sinha

Icahn School of Medicine at Mount Sinai

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William A. Bauman

Icahn School of Medicine at Mount Sinai

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Hiltrud S. Mueller

Albert Einstein College of Medicine

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Susan P. Feldman

Icahn School of Medicine at Mount Sinai

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A. Kumar Sinha

Albert Einstein College of Medicine

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Ann M. Spungen

Icahn School of Medicine at Mount Sinai

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Gregory J. Schilero

Icahn School of Medicine at Mount Sinai

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Jill M. Wecht

Icahn School of Medicine at Mount Sinai

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Michael F. LaFountaine

Icahn School of Medicine at Mount Sinai

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Miroslav Radulovic

Icahn School of Medicine at Mount Sinai

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