Dr. Karen  Chen  Od image

Dr. Karen Chen Od

275 7Th Ave
New York NY 10001
212 911-1709
Medical School: Other - Unknown
Accepts Medicare: No
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: No
License #: TUV007144
NPI: 1235326083
Taxonomy Codes:

Request Appointment Information

Awards & Recognitions

About Us

Practice Philosophy


Medical Malpractice Cases

None Found

Medical Board Sanctions

None Found


None Found


Evaluation of the disco-vertebral junction using ultrashort time-to-echo magnetic resonance imaging: inter-reader agreement and association with vertebral endplate lesions. - Skeletal radiology
To evaluate ultrashort time to echo (UTE) magnetic resonance (MR) morphology of the cartilaginous endplates (CEP) in cadaveric lumbar spines with bony vertebral endplate (VEP) lesions, to determine inter-reader agreement as well as associations between the CEP morphology and VEP lesions as well as other abnormalities.MR imaging of cadaveric lumbar spines from 10 donors was performed at 3T using a UTE MR sequence. Two musculoskeletal radiologists identified the location of vertebral endplate lesions in consensus. The morphology of the CEP overlying the lesions and in the adjacent normal regions was assessed individually. A total of 55 vertebral lesions and 55 normal regions were assessed. The presence of osteophytosis, morphological changes of the anterior and posterior longitudinal ligament, and intervertebral disc signal and morphology was also assessed. Agreement between observers was determined using Cohen's kappa analysis, and association between CEP and vertebral endplate lesions was determined using the chi square test.Fifty-five vertebral endplate lesions were identified and the morphology of CEP evaluated by two readers was in substantial agreement with Cohen's kappa of 0.78. The presence of vertebral endplate abnormality was associated with the presence of osteophytes (39 out of 55 levels), altered morphology and signal of the anterior longitudinal ligament (23 out of 55 levels) and intervertebral discs (30 out of 55 levels).UTE MRI enables evaluation of the CEP with substantial inter-reader agreement. Abnormal changes of the CEP may facilitate formation of lesions of vertebral endplate over time and are associated with degenerative changes of the lumbar spine.
SMN Protein Can Be Reliably Measured in Whole Blood with an Electrochemiluminescence (ECL) Immunoassay: Implications for Clinical Trials. - PloS one
Spinal muscular atrophy (SMA) is caused by defects in the survival motor neuron 1 (SMN1) gene that encodes survival motor neuron (SMN) protein. The majority of therapeutic approaches currently in clinical development for SMA aim to increase SMN protein expression and there is a need for sensitive methods able to quantify increases in SMN protein levels in accessible tissues. We have developed a sensitive electrochemiluminescence (ECL)-based immunoassay for measuring SMN protein in whole blood with a minimum volume requirement of 5μL. The SMN-ECL immunoassay enables accurate measurement of SMN in whole blood and other tissues. Using the assay, we measured SMN protein in whole blood from SMA patients and healthy controls and found that SMN protein levels were associated with SMN2 copy number and were greater in SMA patients with 4 copies, relative to those with 2 and 3 copies. SMN protein levels did not vary significantly in healthy individuals over a four-week period and were not affected by circadian rhythms. Almost half of the SMN protein was found in platelets. We show that SMN protein levels in C/C-allele mice, which model a mild form of SMA, were high in neonatal stage, decreased in the first few weeks after birth, and then remained stable throughout the adult stage. Importantly, SMN protein levels in the CNS correlated with SMN levels measured in whole blood of the C/C-allele mice. These findings have implications for the measurement of SMN protein induction in whole blood in response to SMN-upregulating therapy.
Pharmacokinetics, pharmacodynamics, and efficacy of a small-molecule SMN2 splicing modifier in mouse models of spinal muscular atrophy. - Human molecular genetics
Spinal muscular atrophy (SMA) is caused by the loss or mutation of both copies of the survival motor neuron 1 (SMN1) gene. The relatedSMN2gene is retained, but due to alternative splicing of exon 7, produces insufficient levels of the SMN protein. Here, we systematically characterize the pharmacokinetic and pharmacodynamics properties of the SMN splicing modifier SMN-C1. SMN-C1 is a low-molecular weight compound that promotes the inclusion of exon 7 and increases production of SMN protein in human cells and in two transgenic mouse models of SMA. Furthermore, increases in SMN protein levels in peripheral blood mononuclear cells and skin correlate with those in the central nervous system (CNS), indicating that a change of these levels in blood or skin can be used as a non-invasive surrogate to monitor increases of SMN protein levels in the CNS. Consistent with restored SMN function, SMN-C1 treatment increases the levels of spliceosomal and U7 small-nuclear RNAs and corrects RNA processing defects induced by SMN deficiency in the spinal cord of SMNΔ7 SMA mice. A 100% or greater increase in SMN protein in the CNS of SMNΔ7 SMA mice robustly improves the phenotype. Importantly, a ∼50% increase in SMN leads to long-term survival, but the SMA phenotype is only partially corrected, indicating that certain SMA disease manifestations may respond to treatment at lower doses. Overall, we provide important insights for the translation of pre-clinical data to the clinic and further therapeutic development of this series of molecules for SMA treatment.© The Author 2016. Published by Oxford University Press.
Pharmacologically induced mouse model of adult spinal muscular atrophy to evaluate effectiveness of therapeutics after disease onset. - Human molecular genetics
Spinal muscular atrophy (SMA) is a genetic disease characterized by atrophy of muscle and loss of spinal motor neurons. SMA is caused by deletion or mutation of the survival motor neuron 1 (SMN1) gene, and the nearly identical SMN2 gene fails to generate adequate levels of functional SMN protein due to a splicing defect. Currently, several therapeutics targeted to increase SMN protein are in clinical trials. An outstanding issue in the field is whether initiating treatment in symptomatic older patients would confer a therapeutic benefit, an important consideration as the majority of patients with milder forms of SMA are diagnosed at an older age. An SMA mouse model that recapitulates the disease phenotype observed in adolescent and adult SMA patients is needed to address this important question. We demonstrate here that Δ7 mice, a model of severe SMA, treated with a suboptimal dose of an SMN2 splicing modifier show increased SMN protein, survive into adulthood and display SMA disease-relevant pathologies. Increasing the dose of the splicing modifier after the disease symptoms are apparent further mitigates SMA histopathological features in suboptimally dosed adult Δ7 mice. In addition, inhibiting myostatin using intramuscular injection of AAV1-follistatin ameliorates muscle atrophy in suboptimally dosed Δ7 mice. Taken together, we have developed a new murine model of symptomatic SMA in adolescents and adult mice that is induced pharmacologically from a more severe model and demonstrated efficacy of both SMN2 splicing modifiers and a myostatin inhibitor in mice at later disease stages.© The Author 2016. Published by Oxford University Press. All rights reserved. For Permissions, please email:
Impaired cortical neurogenesis in Plexin-B1 and -B2 double deletion mutant. - Developmental neurobiology
Mammalian cortical expansion is tightly controlled by fine-tuning of proliferation and differentiation of neural progenitors in a region-specific manner. How extrinsic cues interface with cell-intrinsic programs to balance proliferative versus neurogenic decisions remains an unsolved question. We examined the function of Semaphorin receptors Plexin-B1 and -B2 in corticogenesis by generating double mutants, whereby Plexin-B2 was conditionally ablated in the developing brain in a Plexin-B1 null mutant background. Absence of both Plexin-Bs resulted in cortical thinning, particularly in the caudomedial cortex. Plexin-B1/B2 double, but not single, mutants exhibited a reduced neural progenitor pool, attributable to decreased proliferation and an altered division mode favoring cell cycle exit. This resulted in deficient production of neurons throughout the neurogenic period, proportionally affecting all cortical laminae. Consistent with the in vivo data, cultured neural progenitors lacking both Plexin-B1 and -B2 displayed decreased proliferative capacity and increased spontaneous differentiation. Our study therefore defines a novel function of Plexin-B1 and -B2 in transmitting extrinsic signals to maintain proliferative and undifferentiated states of neural progenitors. As single mutants displayed no apparent cortical defects, we conclude that Plexin-B1 and -B2 play redundant or compensatory roles during forebrain development to ensure proper neuronal production and neocortical expansion. This article is protected by copyright. All rights reserved.© 2015 Wiley Periodicals, Inc.
Biomarker for Spinal Muscular Atrophy: Expression of SMN in Peripheral Blood of SMA Patients and Healthy Controls. - PloS one
Spinal muscular atrophy is caused by a functional deletion of SMN1 on Chromosome 5, which leads to a progressive loss of motor function in affected patients. SMA patients have at least one copy of a similar gene, SMN2, which produces functional SMN protein, although in reduced quantities. The severity of SMA is variable, partially due to differences in SMN2 copy numbers. Here, we report the results of a biomarker study characterizing SMA patients of varying disease severity. SMN copy number, mRNA and Protein levels in whole blood of patients were measured and compared against a cohort of healthy controls. The results show differential regulation of expression of SMN2 in peripheral blood between patients and healthy subjects.
Evaluation of older driver head functional range of motion using portable immersive virtual reality. - Experimental gerontology
The number of drivers over 65 years of age continues to increase. Although neck rotation range has been identified as a factor associated with self-reported crash history in older drivers, it was not consistently reported as indicators of older driver performance or crashes across previous studies. It is likely that drivers use neck and trunk rotation when driving, and therefore the functional range of motion (ROM) (i.e. overall rotation used during a task) of older drivers should be further examined.Evaluate older driver performance in an immersive virtual reality, simulated, dynamic driving blind spot target detection task.A cross-sectional laboratory study recruited twenty-six licensed drivers (14 young between 18 and 35 years, and 12 older between 65 to 75 years) from the local community. Participants were asked to detect targets by performing blind spot check movements while neck and trunk rotation was tracked. Functional ROM, target detection success, and time to detection were analyzed.In addition to neck rotation, older and younger drivers on average rotated their trunks 9.96° and 18.04°, respectively. The younger drivers generally demonstrated 15.6° greater functional ROM (p<.001), were nearly twice as successful in target detection due to target location (p=.008), and had 0.46 s less target detection time (p=.016) than the older drivers.Assessing older driver functional ROM may provide more comprehensive assessment of driving ability than neck ROM. Target detection success and time to detection may also be part of the aging process as these measures differed between driver groups.Copyright © 2015 Elsevier Inc. All rights reserved.
MR imaging findings of trigger thumb. - Skeletal radiology
Trigger finger (or trigger thumb), also known as sclerosing tenosynovitis, is a common clinical diagnosis that rarely presents for imaging. Because of this selection bias, many radiologists may not be familiar with the process. Furthermore, patients who do present for imaging frequently have misleading examination indications. To our knowledge, magnetic resonance (MR) imaging findings of trigger thumb have not been previously reported in the literature. In this article, we review the entity of trigger thumb, the anatomy involved, and associated imaging findings, which include flexor pollicis longus tendinosis with a distinct nodule, A1 pulley thickening, and tenosynovitis. In addition, in some cases, an abnormal Av pulley is apparent. In the rare cases of trigger finger that present for MR imaging, accurate diagnosis by the radiologist can allow initiation of treatment and avoid further unnecessary workup.
Virtual exertions: evoking the sense of exerting forces in virtual reality using gestures and muscle activity. - Human factors
This study was a proof of concept for virtual exertions, a novel method that involves the use of body tracking and electromyography for grasping and moving projections of objects in virtual reality (VR). The user views objects in his or her hands during rehearsed co-contractions of the same agonist-antagonist muscles normally used for the desired activities to suggest exerting forces.Unlike physical objects, virtual objects are images and lack mass. There is currently no practical physically demanding way to interact with virtual objects to simulate strenuous activities.Eleven participants grasped and lifted similar physical and virtual objects of various weights in an immersive 3-D Cave Automatic Virtual Environment. Muscle activity, localized muscle fatigue, ratings of perceived exertions, and NASA Task Load Index were measured. Additionally, the relationship between levels of immersion (2-D vs. 3-D) was studied.Although the overall magnitude of biceps activity and workload were greater in VR, muscle activity trends and fatigue patterns for varying weights within VR and physical conditions were the same. Perceived exertions for varying weights were not significantly different between VR and physical conditions.Perceived exertion levels and muscle activity patterns corresponded to the assigned virtual loads, which supported the hypothesis that the method evoked the perception of physical exertions and showed that the method was promising.Ultimately this approach may offer opportunities for research and training individuals to perform strenuous activities under potentially safer conditions that mimic situations while seeing their own body and hands relative to the scene.© 2014, Human Factors and Ergonomics Society.
Dual Element Intercalation into 2D Layered Bi₂Se₃ Nanoribbons. - Journal of the American Chemical Society
We demonstrate the intercalation of multiple zero-valent atomic species into two-dimensional (2D) layered Bi2Se3 nanoribbons. Intercalation is performed chemically through a stepwise combination of disproportionation redox reactions, hydrazine reduction, or carbonyl decomposition. Traditional intercalation is electrochemical thus limiting intercalant guests to a single atomic species. We show that multiple zero-valent atoms can be intercalated through this chemical route into the host lattice of a 2D crystal. Intermetallic species exhibit unique structural ordering demonstrated in a variety of superlattice diffraction patterns. We believe this method is general and can be used to achieve a wide variety of new 2D materials previously inaccessible.

Map & Directions

275 7Th Ave New York, NY 10001
View Directions In Google Maps

Nearby Doctors

133 W 25Th St #3
New York, NY 10001
516 953-3925
12 W 27Th St 9Th Floor
New York, NY 10001
212 759-9355
430 W 34Th Street, 16K
New York, NY 10001
646 421-1551
276 5Th Ave Suite 307A
New York, NY 10001
646 067-7156
460 West 34Th Street
New York, NY 10001
212 736-6519
307 Seventh Avenue Suite 1402
New York, NY 10001
908 463-3232
220 5Th Ave Suite 802
New York, NY 10001
347 612-2557
460 W 34Th St
New York, NY 10001
212 736-6100
276 5Th Ave Suite 307A
New York, NY 10001
917 536-6517
460 West 34Th Street 9Th Floor
New York, NY 10001
212 736-6519