Docality.com Logo
 
Dr. Raj  Murali  Md image

Dr. Raj Murali Md

19 Bradhurst Ave Suite 2800
Hawthorne NY 10532
914 458-8111
Medical School: Other - 1968
Accepts Medicare: Yes
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: No
License #: 126605-1
NPI: 1902891831
Taxonomy Codes:
174400000X

Request Appointment Information

Awards & Recognitions

About Us

Practice Philosophy

Conditions

Dr. Raj Murali is associated with these group practices

Procedure Pricing

HCPCS Code Description Average Price Average Price
Allowed By Medicare
HCPCS Code:99291 Description:Critical care first hour Average Price:$1,202.00 Average Price Allowed
By Medicare:
$240.88
HCPCS Code:99204 Description:Office/outpatient visit new Average Price:$438.00 Average Price Allowed
By Medicare:
$182.76
HCPCS Code:99214 Description:Office/outpatient visit est Average Price:$260.00 Average Price Allowed
By Medicare:
$118.56
HCPCS Code:99213 Description:Office/outpatient visit est Average Price:$180.00 Average Price Allowed
By Medicare:
$80.46

HCPCS Code Definitions

99291
Critical care, evaluation and management of the critically ill or critically injured patient; first 30-74 minutes
99214
Office or other outpatient visit for the evaluation and management of an established patient, which requires at least 2 of these 3 key components: A detailed history; A detailed examination; Medical decision making of moderate complexity. Counseling and/or coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of moderate to high severity. Typically, 25 minutes are spent face-to-face with the patient and/or family.
99213
Office or other outpatient visit for the evaluation and management of an established patient, which requires at least 2 of these 3 key components: An expanded problem focused history; An expanded problem focused examination; Medical decision making of low complexity. Counseling and coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of low to moderate severity. Typically, 15 minutes are spent face-to-face with the patient and/or family.
99204
Office or other outpatient visit for the evaluation and management of a new patient, which requires these 3 key components: A comprehensive history; A comprehensive examination; Medical decision making of moderate complexity. Counseling and/or coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of moderate to high severity. Typically, 45 minutes are spent face-to-face with the patient and/or family.

Medical Malpractice Cases

None Found

Medical Board Sanctions

None Found

Referrals

NPI
Doctor Name
Specialty
Count
1902834286
Diagnostic Radiology
220
1003868365
Diagnostic Radiology
169
1679551923
Diagnostic Radiology
156
1871593137
Neurology
136
1477613032
Diagnostic Radiology
124
1447257514
Diagnostic Radiology
123
1245267889
Diagnostic Radiology
79
1104826395
Neurology
74
1881617504
Pulmonary Disease
44
1760559959
Neurology
40
*These referrals represent the top 10 that Dr. Murali has made to other doctors

Publications

Molecular Pathways Mediating Metastases to the Brain via Epithelial-to-Mesenchymal Transition: Genes, Proteins, and Functional Analysis. - Anticancer research
Brain metastases are the leading cause of morbidity and mortality among patients with disseminated cancer. The development of metastatic disease involves an orderly sequence of steps enabling tumor cells to migrate from the primary tumor and colonize at secondary locations. In order to achieve this complex metastatic potential, a cancer cell is believed to undergo a cellular reprogramming process involving the development of a degree of stemness, via a proposed process termed epithelial-to-mesenchymal transition (EMT). Upon reaching its secondary site, these reprogrammed cancer stem cells submit to a reversal process designated mesenchymal-to-epithelial transition (MET), enabling establishment of metastases. Here, we examined the expression of markers of EMT, MET, and stem cells in metastatic brain tumor samples.Immunohistochemical analyses were performed to establish the markers of EMT and MET. Co-expression of these markers was determined by immunofluorescence analysis. Gene-expression analysis was conducted using tissues from brain metastases of primary adenocarcinoma of the lung compared to non-metastatic tissue. Cell proliferation was carried out using 3- (4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide S-phase entry analysis, by determining the 5-ethynyl-2'-deoxyuridine incorporation. Scratch wound and chemotactic migration assays were performed in an astrocytic setting.Metastatic brain tumor samples displayed expression of epithelial markers (zinc finger protein SNAI1 and Twist-related protein-1), as well as the mesenchymal marker vimentin. The stem cell marker CD44 was also highly expressed. Moreover, co-expression of the epithelial marker E-cadherin with the mesenchymal marker vimentin was evident, suggesting a state of transition. Expression analysis of transcription factor genes in metastatic brain tumor samples demonstrated an alteration in genes associated with neurogenesis, differentiation, and reprogramming. Furthermore, tumor cells grown in astrocytic medium displayed increased cell proliferation and enhanced S-phase cell-cycle entry. Additionally, chemotactic signaling from the astrocytic environment promoted tumor cell migration. Primary tumor cells and astrocytes were also shown to grow amicably together, forming cell-to-cell interactions.These findings suggest that cellular reprogramming via EMT/MET plays a critical step in the formation of brain metastases, where the cerebral milieu provides a microenvironment suitable for the development of metastatic disease.Copyright© 2016 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.
The Anti-Inflammatory Compound Curcumin Enhances Locomotor and Sensory Recovery after Spinal Cord Injury in Rats by Immunomodulation. - International journal of molecular sciences
Well known for its anti-oxidative and anti-inflammation properties, curcumin is a polyphenol found in the rhizome of Curcuma longa. In this study, we evaluated the effects of curcumin on behavioral recovery, glial scar formation, tissue preservation, axonal sprouting, and inflammation after spinal cord injury (SCI) in male Wistar rats. The rats were randomized into two groups following a balloon compression injury at the level of T9-T10 of the spinal cord, namely vehicle- or curcumin-treated. Curcumin was applied locally on the surface of the injured spinal cord immediately following injury and then given intraperitoneally daily; the control rats were treated with vehicle in the same manner. Curcumin treatment improved behavioral recovery within the first week following SCI as evidenced by improved Basso, Beattie, and Bresnahan (BBB) test and plantar scores, representing locomotor and sensory performance, respectively. Furthermore, curcumin treatment decreased glial scar formation by decreasing the levels of MIP1α, IL-2, and RANTES production and by decreasing NF-κB activity. These results, therefore, demonstrate that curcumin has a profound anti-inflammatory therapeutic potential in the treatment of spinal cord injury, especially when given immediately after the injury.
ATP-site binding inhibitor effectively targets mTORC1 and mTORC2 complexes in glioblastoma. - International journal of oncology
The PI3K-AKT-mTOR signaling axis is central to the transformed phenotype of glioblastoma (GBM) cells, due to frequent loss of tumor suppressor PTEN (phosphatase and tensin homolog deleted on chromosome 10). The mechanistic target of rapamycin (mTOR) kinase is present in two cellular multi-protein complexes, mTORC1 and mTORC2, which have distinct subunit composition, substrates and mechanisms of action. Targeting the mTOR protein is a promising strategy for GBM therapy. However, neither of these complexes is fully inhibited by the allosteric inhibitor of mTOR, rapamycin or its analogs. Herein, we provide evidence that the combined inhibition of mTORC1/2, using the ATP-competitive binding inhibitor PP242, would effectively suppress GBM growth and dissemination as compared to an allosteric binding inhibitor of mTOR. GBM cells treated with PP242 demonstrated significantly decreased activation of mTORC1 and mTORC2, as shown by reduced phosphorylation of their substrate levels, p70 S6KThr389 and AKTSer473, respectively, in a dose-dependent manner. Furthermore, insulin induced activation of these kinases was abrogated by pretreatment with PP242 as compared with rapamycin. Unlike rapamycin, PP242 modestly activates extracellular regulated kinase (ERK1/2), as shown by expression of pERKThr202/Tyr204. Cell proliferation and S-phase entry of GBM cells was significantly suppressed by PP242, which was more pronounced compared to rapamycin treatment. Lastly, PP242 significantly suppressed the migration of GBM cells, which was associated with a change in cellular behavior rather than cytoskeleton loss. In conclusion, these results underscore the potential therapeutic use of the PP242, a novel ATP-competitive binding inhibitor of mTORC1/2 kinase, in suppression of GBM growth and dissemination.
Metastatic Renal Cell Carcinoma Mimicking Trigeminal Schwannoma in a Patient Presenting with Trigeminal Neuralgia. - Journal of neurological surgery reports
We present an unusual case of a metastatic renal cell carcinoma (RCC) mimicking trigeminal schwannoma. The patient, with no prior history of RCC, presented with clinical symptoms and imaging consistent with trigeminal neuralgia secondary to trigeminal schwannoma. Magnetic resonance imaging of the brain showed a large bilobed cystic/solid mass primarily in the cerebellopontine angle cistern, with extension into the left middle cranial fossa, Meckel cave, and left cavernous sinus. Following surgical excision, histopathology revealed the tumor to be an RCC infiltrating into the trigeminal nerve fascicles. Further imaging and investigation revealed widespread metastasis to the vertebral bodies and long bones. Metastatic RCC to the trigeminal nerve is rare. Despite the development of more effective treatment modalities, the prognosis of metastatic RCC remains poor. To our knowledge, this is the first reported case of RCC metastasizing to the trigeminal nerve fascicles.
The long-term outcome of four-corner fusion. - Journal of wrist surgery
Introduction Four-corner arthrodesis with excision of the scaphoid is an accepted salvage procedure for scapholunate advanced collapse (SLAC) and scaphoid nonunion advanced collapse (SNAC) and has been performed in our unit for over 20 years. We have undertaken a retrospective review of 116 of these procedures performed in 110 patients between 1992 and 2009. Fifty-eight patients attended for a clinical evaluation, and 29 responded by postal questionnaire. Methods The surgical technique undertaken was standard. That is, through a dorsal approach the scaphoid and tip of the radial styloid were excised. The capitate, lunate, triquetrum, and hamate articular surfaces were then prepared down to bleeding bone. Bone grafts from the scaphoid and radial styloid were then inserted and fixation undertaken. For the latter, various methods were used, including Kirschner (K-)wires, staples, bone screws, but predominantly the Spider plate (Integra Life Sciences, USA). Thereafter the wrist was immobilized for a minimum period of 2 weeks prior to rehabilitation. Results Follow-up was done at a mean of 9 years and 4 months (range 3-19 years). All patients reported a significant improvement in pain relief and ∼50% of flexion extension, although only 40% of radioulnar deviation. Grip strength was again ∼50% of the contralateral side. Most patients reported a significant improvement in function with 87% returning to work. In addition, radiologic evaluation identified 28 patients (31%) who demonstrated ongoing signs of nonunion, particularly around the triquetrum. Fourteen of these (15%) underwent a further procedure, generally with success. Finally, none of the patients demonstrated any arthritic changes in the lunate fossa on follow-up X-ray, and all secondary procedures were undertaken within 2 years of the primary. Discussion This research has demonstrated that four-corner fusion fixed with a circular plate can result in a satisfactory outcome with a reduction in pain, a functional range of motion, and a satisfactory functional outcome. The bulk of the complications appear to occur in the first 2 years after surgery. Thereafter, analysis shows long-term satisfaction with little deterioration. Nonunion, particularly around the triquetrum, continues to be a problem, but it may be that this bone should be excised along with the scaphoid, resulting in a three-part fusion only. Alternatively, a simple capitolunate fusion may be satisfactory.
Glioblastoma: molecular pathways, stem cells and therapeutic targets. - Cancers
Glioblastoma (GBM), a WHO-defined Grade IV astrocytoma, is the most common and aggressive CNS malignancy. Despite current treatment modalities, the survival time remains dismal. The main cause of mortality in patients with this disease is reoccurrence of the malignancy, which is attributed to treatment-resistant cancer stem cells within and surrounding the primary tumor. Inclusion of novel therapies, such as immuno- and DNA-based therapy, may provide better means of treating GBM. Furthermore, manipulation of recently discovered non-coding microRNAs, some of which regulate tumor growth through the development and maintenance of GBM stem cells, could provide new prospective therapies. Studies conducted by The Cancer Genome Atlas (TCGA) also demonstrate the role of molecular pathways, specifically the activated PI3K/AKT/mTOR pathway, in GBM tumorigenesis. Inhibition of the aforementioned pathway may provide a more direct and targeted method to GBM treatment. The combination of these treatment modalities may provide an innovative therapeutic approach for the management of GBM.
Involvement of mTOR signaling pathways in regulating growth and dissemination of metastatic brain tumors via EMT. - Anticancer research
Metastatic dissemination to the brain may involve a process termed epithelial-mesenchymal transition (EMT), which results in a migratory, invasive and proliferative cell phenotype. Recent studies suggest that Mechanistic target of rapamycin (mTOR, that exists in two multi-protein complexes (mTORC1 and mTORC2), may regulate EMT, in addition to controlling cell growth, survival, metabolism and motility. However, the role of mTOR in brain metastases remains elusive. We hypothesize that mTOR plays a crucial role in the process of EMT in brain metastasis and therefore serves as a target of therapy.Immunohistochemical analyses were performed to determine the expression of components of mTOR pathways. Immunofluorescence and immunoblotting were executed to determine the markers of EMT after treatments with siRNA or inhibitors of mTOR pathways. Cell proliferation using MTT, S-phase entry by determining EdU-incorporation, chemotactic and scratch-wound migration assays were performed.Metastatic tumor samples expressed components of mTOR pathways, namely, mTOR, Raptor and Rictor with a significant overlap. Metastatic potential was enhanced in an astrocytic environment and suppressed following mTOR inhibition. mTOR inhibition resulted in nuclear localization of the epithelial marker of EMT, E-cadherin, and enhancement in expression of the mesenchymal marker vimentin.Results suggest that the mTOR pathway is activated in metastatic brain tumors, and inhibition of mTOR signaling could provide therapeutic value in the management of patients with brain metastases.Copyright© 2015 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.
Cerebrospinal fluid leaks and encephaloceles of temporal bone origin: nuances to diagnosis and management. - World neurosurgery
Temporal bone encephalocele has become less common as the incidence of chronic mastoid infection and surgery for this condition has decreased. As a result, the diagnosis is often delayed, and the encephalocele is often an incidental finding. This situation can result in serious neurologic complications with patients presenting with cerebrospinal fluid leak and meningitis. We review the occurrence of, characteristics of, and repair experience with temporal encephaloceles from 2000-2012.We conducted a retrospective review of 32 patients undergoing combined mastoidectomy and middle cranial fossa craniotomy for the treatment of temporal encephalocele.The diagnosis of temporal encephalocele was made in all patients using high-resolution temporal bone computed tomography and magnetic resonance imaging. At the time of diagnosis, 12 patients had confirmed cerebrospinal fluid leak; other common presenting symptoms included hearing loss and ear fullness. Tegmen defect was most commonly due to chronic otitis media (n = 14). Of these patients, 8 had undergone prior mastoidectomy, suggesting an iatrogenic cause. Other etiologies included radiation exposure, congenital defects, and spontaneous defects. Additionally, 2 patients presented with meningitis; 1 patient had serious neurologic deficits resulting from venous infarction.The risk of severe neurologic complications after the herniation of intracranial contents through a tegmen defect necessitates prompt recognition and appropriate management. Computed tomography and magnetic resonance imaging aid in definitive diagnosis. A combined mastoid/middle fossa approach allows for sustainable repair with adequate exposure of defects and support of intracranial contents.Copyright © 2015 Elsevier Inc. All rights reserved.
Distinct signaling mechanisms of mTORC1 and mTORC2 in glioblastoma multiforme: a tale of two complexes. - Advances in biological regulation
Mechanistic target of rapamycin (mTOR) is a serine-threonine kinase that functions via two multiprotein complexes, namely mTORC1 and mTORC2, each characterized by different binding partners that confer separate functions. mTORC1 function is tightly regulated by PI3-K/Akt and is sensitive to rapamycin. mTORC2 is sensitive to growth factors, not nutrients, and is associated with rapamycin-insensitivity. mTORC1 regulates protein synthesis and cell growth through downstream molecules: 4E-BP1 (also called EIF4E-BP1) and S6K. Also, mTORC2 is thought to modulate growth factor signaling by phosphorylating the C-terminal hydrophobic motif of some AGC kinases such as Akt and SGK. Recent evidence has suggested that mTORC2 may play an important role in maintenance of normal as well as cancer cells by virtue of its association with ribosomes, which may be involved in metabolic regulation of the cell. Rapamycin (sirolimus) and its analogs known as rapalogues, such as RAD001 (everolimus) and CCI-779 (temsirolimus), suppress mTOR activity through an allosteric mechanism that acts at a distance from the ATP-catalytic binding site, and are considered incomplete inhibitors. Moreover, these compounds suppress mTORC1-mediated S6K activation, thereby blocking a negative feedback loop, leading to activation of mitogenic pathways promoting cell survival and growth. Consequently, mTOR is a suitable target of therapy in cancer treatments. However, neither of these complexes is fully inhibited by the allosteric inhibitor rapamycin or its analogs. In recent years, new pharmacologic agents have been developed which can inhibit these complexes via ATP-binding mechanism, or dual inhibition of the canonical PI3-K/Akt/mTOR signaling pathway. These compounds include WYE-354, KU-003679, PI-103, Torin1, and Torin2, which can target both complexes or serve as a dual inhibitor for PI3-K/mTOR. This investigation describes the mechanism of action of pharmacological agents that effectively target mTORC1 and mTORC2 resulting in suppression of growth, proliferation, and migration of tumor and cancer stem cells.Copyright © 2014. Published by Elsevier Ltd.
Human mesenchymal stem cells modulate inflammatory cytokines after spinal cord injury in rat. - International journal of molecular sciences
Transplantation of mesenchymal stem cells (MSC) improves functional recovery in experimental models of spinal cord injury (SCI); however, the mechanisms underlying this effect are not completely understood. We investigated the effect of intrathecal implantation of human MSC on functional recovery, astrogliosis and levels of inflammatory cytokines in rats using balloon-induced spinal cord compression lesions. Transplanted cells did not survive at the lesion site of the spinal cord; however, functional recovery was enhanced in the MSC-treated group as was confirmed by the Basso, Beattie, and Bresnahan (BBB) and the flat beam test. Morphometric analysis showed a significantly higher amount of remaining white matter in the cranial part of the lesioned spinal cords. Immunohistochemical analysis of the lesions indicated the rearrangement of the glial scar in MSC-treated animals. Real-time PCR analysis revealed an increased expression of Irf5, Mrc1, Fgf2, Gap43 and Gfap. Transplantation of MSCs into a lesioned spinal cord reduced TNFα, IL-4, IL-1β, IL-2, IL-6 and IL-12 and increased the levels of MIP-1α and RANTES when compared to saline-treated controls. Intrathecal implantation of MSCs reduces the inflammatory reaction and apoptosis, improves functional recovery and modulates glial scar formation after SCI, regardless of cell survival. Therefore, repeated applications may prolong the beneficial effects induced by MSC application.

Map & Directions

19 Bradhurst Ave Suite 2800 Hawthorne, NY 10532
View Directions In Google Maps

Nearby Doctors

19 Bradhurst Ave Suite 3040N
Hawthorne, NY 10532
914 936-6820
19 Bradhurst Ave Ste 1400
Hawthorne, NY 10532
914 944-4370
19 Bradhurst Ave Suite 3070N
Hawthorne, NY 10532
914 727-7887
19 Bradhurst Ave Suite 200N
Hawthorne, NY 10532
914 937-7701
19 Bradhurst Ave Ste. 1400
Hawthorne, NY 10532
914 670-0000
19 Bradhurst Ave Suite 700
Hawthorne, NY 10532
914 373-3500
19 Bradhurst Ave Suite 200N
Hawthorne, NY 10532
914 937-7701
19 Bradhurst Ave Suite 1900
Hawthorne, NY 10532
914 471-1958
19 Bradhurst Ave Ste. 1400
Hawthorne, NY 10532
914 938-8333