2131 W 3Rd St
Los Angeles CA 90057
Medical School: Other - 1990
Accepts Medicare: Yes
Participates In eRX: No
Participates In PQRS: Yes
Participates In EHR: No
License #: A85887
Taxonomy Codes:207ZC0500X 207ZP0102X
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Awards & Recognitions
Dr. Hongying Tan is associated with these group practices
|HCPCS Code||Description||Average Price||Average Price
Allowed By Medicare
|HCPCS Code:38221||Description:Bone marrow biopsy||Average Price:$400.00||Average Price Allowed
|HCPCS Code:88309||Description:Tissue exam by pathologist||Average Price:$390.00||Average Price Allowed
|HCPCS Code:88331||Description:Path consult intraop 1 bloc||Average Price:$210.00||Average Price Allowed
|HCPCS Code:88305||Description:Tissue exam by pathologist||Average Price:$175.00||Average Price Allowed
|HCPCS Code:88304||Description:Tissue exam by pathologist||Average Price:$120.00||Average Price Allowed
|HCPCS Code:88307||Description:Tissue exam by pathologist||Average Price:$190.00||Average Price Allowed
|HCPCS Code:88302||Description:Tissue exam by pathologist||Average Price:$112.00||Average Price Allowed
|HCPCS Code:88329||Description:Path consult introp||Average Price:$125.00||Average Price Allowed
|HCPCS Code:85097||Description:Bone marrow interpretation||Average Price:$105.00||Average Price Allowed
|HCPCS Code:88173||Description:Cytopath eval fna report||Average Price:$128.00||Average Price Allowed
|HCPCS Code:86077||Description:Physician blood bank service||Average Price:$105.00||Average Price Allowed
|HCPCS Code:88342||Description:Immunohistochemistry||Average Price:$95.00||Average Price Allowed
|HCPCS Code:88300||Description:Surgical path gross||Average Price:$50.00||Average Price Allowed
|HCPCS Code:88312||Description:Special stains group 1||Average Price:$60.00||Average Price Allowed
|HCPCS Code:88112||Description:Cytopath cell enhance tech||Average Price:$90.00||Average Price Allowed
|HCPCS Code:88313||Description:Special stains group 2||Average Price:$42.00||Average Price Allowed
|HCPCS Code:85060||Description:Blood smear interpretation||Average Price:$50.00||Average Price Allowed
|HCPCS Code:88311||Description:Decalcify tissue||Average Price:$22.00||Average Price Allowed
HCPCS Code Definitions
- Blood smear, peripheral, interpretation by physician with written report
- Bone marrow; biopsy, needle or trocar
- Cytopathology, evaluation of fine needle aspirate; interpretation and report
- Blood bank physician services; difficult cross match and/or evaluation of irregular antibody(s), interpretation and written report
- Level III - Surgical pathology, gross and microscopic examination Abortion, induced Abscess Aneurysm - arterial/ventricular Anus, tag Appendix, other than incidental Artery, atheromatous plaque Bartholin's gland cyst Bone fragment(s), other than pathologic fracture Bursa/synovial cyst Carpal tunnel tissue Cartilage, shavings Cholesteatoma Colon, colostomy stoma Conjunctiva - biopsy/pterygium Cornea Diverticulum - esophagus/small intestine Dupuytren's contracture tissue Femoral head, other than fracture Fissure/fistula Foreskin, other than newborn Gallbladder Ganglion cyst Hematoma Hemorrhoids Hydatid of Morgagni Intervertebral disc Joint, loose body Meniscus Mucocele, salivary Neuroma - Morton's/traumatic Pilonidal cyst/sinus Polyps, inflammatory - nasal/sinusoidal Skin - cyst/tag/debridement Soft tissue, debridement Soft tissue, lipoma Spermatocele Tendon/tendon sheath Testicular appendage Thrombus or embolus Tonsil and/or adenoids Varicocele Vas deferens, other than sterilization Vein, varicosity
- Level IV - Surgical pathology, gross and microscopic examination Abortion - spontaneous/missed Artery, biopsy Bone marrow, biopsy Bone exostosis Brain/meninges, other than for tumor resection Breast, biopsy, not requiring microscopic evaluation of surgical margins Breast, reduction mammoplasty Bronchus, biopsy Cell block, any source Cervix, biopsy Colon, biopsy Duodenum, biopsy Endocervix, curettings/biopsy Endometrium, curettings/biopsy Esophagus, biopsy Extremity, amputation, traumatic Fallopian tube, biopsy Fallopian tube, ectopic pregnancy Femoral head, fracture Fingers/toes, amputation, non-traumatic Gingiva/oral mucosa, biopsy Heart valve Joint, resection Kidney, biopsy Larynx, biopsy Leiomyoma(s), uterine myomectomy - without uterus Lip, biopsy/wedge resection Lung, transbronchial biopsy Lymph node, biopsy Muscle, biopsy Nasal mucosa, biopsy Nasopharynx/oropharynx, biopsy Nerve, biopsy Odontogenic/dental cyst Omentum, biopsy Ovary with or without tube, non-neoplastic Ovary, biopsy/wedge resection Parathyroid gland Peritoneum, biopsy Pituitary tumor Placenta, other than third trimester Pleura/pericardium - biopsy/tissue Polyp, cervical/endometrial Polyp, colorectal Polyp, stomach/small intestine Prostate, needle biopsy Prostate, TUR Salivary gland, biopsy Sinus, paranasal biopsy Skin, other than cyst/tag/debridement/plastic repair Small intestine, biopsy Soft tissue, other than tumor/mass/lipoma/debridement Spleen Stomach, biopsy Synovium Testis, other than tumor/biopsy/castration Thyroglossal duct/brachial cleft cyst Tongue, biopsy Tonsil, biopsy Trachea, biopsy Ureter, biopsy Urethra, biopsy Urinary bladder, biopsy Uterus, with or without tubes and ovaries, for prolapse Vagina, biopsy Vulva/labia, biopsy
- Bone marrow, smear interpretation
- Cytopathology, selective cellular enhancement technique with interpretation (eg, liquid based slide preparation method), except cervical or vaginal
- Level II - Surgical pathology, gross and microscopic examination Appendix, incidental Fallopian tube, sterilization Fingers/toes, amputation, traumatic Foreskin, newborn Hernia sac, any location Hydrocele sac Nerve Skin, plastic repair Sympathetic ganglion Testis, castration Vaginal mucosa, incidental Vas deferens, sterilization
- Level I - Surgical pathology, gross examination only
- Level V - Surgical pathology, gross and microscopic examination Adrenal, resection Bone - biopsy/curettings Bone fragment(s), pathologic fracture Brain, biopsy Brain/meninges, tumor resection Breast, excision of lesion, requiring microscopic evaluation of surgical margins Breast, mastectomy - partial/simple Cervix, conization Colon, segmental resection, other than for tumor Extremity, amputation, non-traumatic Eye, enucleation Kidney, partial/total nephrectomy Larynx, partial/total resection Liver, biopsy - needle/wedge Liver, partial resection Lung, wedge biopsy Lymph nodes, regional resection Mediastinum, mass Myocardium, biopsy Odontogenic tumor Ovary with or without tube, neoplastic Pancreas, biopsy Placenta, third trimester Prostate, except radical resection Salivary gland Sentinel lymph node Small intestine, resection, other than for tumor Soft tissue mass (except lipoma) - biopsy/simple excision Stomach - subtotal/total resection, other than for tumor Testis, biopsy Thymus, tumor Thyroid, total/lobe Ureter, resection Urinary bladder, TUR Uterus, with or without tubes and ovaries, other than neoplastic/prolapse
- Level VI - Surgical pathology, gross and microscopic examination Bone resection Breast, mastectomy - with regional lymph nodes Colon, segmental resection for tumor Colon, total resection Esophagus, partial/total resection Extremity, disarticulation Fetus, with dissection Larynx, partial/total resection - with regional lymph nodes Lung - total/lobe/segment resection Pancreas, total/subtotal resection Prostate, radical resection Small intestine, resection for tumor Soft tissue tumor, extensive resection Stomach - subtotal/total resection for tumor Testis, tumor Tongue/tonsil -resection for tumor Urinary bladder, partial/total resection Uterus, with or without tubes and ovaries, neoplastic Vulva, total/subtotal resection
- Pathology consultation during surgery
- Special stain including interpretation and report; Group II, all other (eg, iron, trichrome), except stain for microorganisms, stains for enzyme constituents, or immunocytochemistry and immunohistochemistry
- Decalcification procedure (List separately in addition to code for surgical pathology examination)
- Special stain including interpretation and report; Group I for microorganisms (eg, acid fast, methenamine silver)
- Immunohistochemistry or immunocytochemistry, each separately identifiable antibody per block, cytologic preparation, or hematologic smear; first separately identifiable antibody per slide
- Pathology consultation during surgery; first tissue block, with frozen section(s), single specimen
Medical Malpractice Cases
Medical Board Sanctions
*These referrals represent the top 10 that Dr. Tan has made to other doctors
Transfusion of Old RBCs Induces Neuroinflammation and Cognitive Impairment. - Critical care medicine
Transfusing RBCs stored for longer than 14 days (old RBC) in humans is common. This transfusion can injure organs, such as lungs and kidneys. We determined whether transfusion with old RBC injured brain.Prospective, controlled animal study.University research laboratory.Adult male Sprague-Dawley rats.Six-month-old Sprague-Dawley rats lost 20% total blood volume and then received RBC prepared from equal volume of the lost blood. RBC was stored for 1 day (fresh RBC) or 7 days (old RBC, storage lesions similar to those of human RBC stored for 28 d). Some rats received IV cell-free hemoglobin. These rats were not subjected to hemorrhage and RBC transfusion.Rats were subjected to Barnes maze and fear conditioning tests from 1 week after blood transfusion. Rats transfused with old RBC but not fresh RBC took a longer time to identify the target hole in the Barnes maze and had less context-related fear conditioning behavior than control rats. Old RBC significantly increased interleukin 6 and ionized calcium-binding adapter molecule 1 in the hippocampus at 24 hours after the transfusion. These effects were attenuated by sulforaphane and minocycline, an antibiotic with anti-inflammatory property. Old RBC solution had a higher concentration of cell-free hemoglobin. Sulforaphane increased haptoglobin, a chelator of cell-free hemoglobin. Rats that received cell-free hemoglobin had a pattern of neuroinflammation and impairment of learning and memory similar to that of rats that received old RBC.These results provide initial evidence to suggest that transfusion of old RBC induces neuroinflammation and impairment of learning and memory. These effects may be mediated by cell-free hemoglobin.
The choice of general anesthetics may not affect neuroinflammation and impairment of learning and memory after surgery in elderly rats. - Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology
Postoperative cognitive dysfunction (POCD) often occurs in elderly patients and may involve neuroinflammation. This study was to determine whether anesthetic choice (intravenous vs. volatile anesthetics) affects cognitive impairment and neuroinflammation in elderly rat. Total 54 twenty-month old male Fischer 344 rats were assigned randomly to control, right carotid exposure under propofol-buprenorphine or isoflurane-buprenorphine anesthesia groups. They were tested by Barnes maze and fear conditioning from 6 days after the surgery. Their brains were harvested 24 h after the surgery for quantifying interleukin (IL) 1Î², tumor necrosis factor (TNF)Î± and ionized calcium binding adaptor molecule 1 (Iba-1). We showed that the heart rates and mean arterial blood pressure were similar during surgery under propofol-buprenorphine or isoflurane-buprenorphine anesthesia. There was no difference in the surgery-induced increase of the plasma IL-1Î² and TNFÎ± levels under these two types of anesthesia. Rats subjected to surgery took longer than control rats to identify the target hole 8 days after the completion of training sessions in Barnes maze [32â€‰Â±â€‰23 s for control, 118â€‰Â±â€‰64 s for propofol group (Pâ€‰<â€‰0.05 vs. control), 107â€‰Â±â€‰64 s for isoflurane group (Pâ€‰<â€‰0.05 vs. control)] and had less freezing behavior in the fear conditioning test. Surgery and anesthesia increased IL-1Î² and Iba-1 but did not affect tau phosphorylated at S199/202 and S396 in the cerebral cortex and hippocampus. Our results suggest that surgery under general anesthesia induces neuroinflammation and cognitive impairment. Anesthetic choice may not be a significant modifiable factor for these effects.
Amantadine alleviates postoperative cognitive dysfunction possibly by increasing glial cell line-derived neurotrophic factor in rats. - Anesthesiology
Postoperative cognitive dysfunction is a clinical entity that is associated with poor outcome. We determined the effectiveness of amantadine in reducing surgery-induced cognitive impairment and the role of glial cell line-derived neurotrophic factor (GDNF) in this effect.Four-month old male Fischer 344 rats were subjected to right carotid exposure under intravenous anesthesia. Some rats received intraperitoneal injection of 25 mg/kg/day amantadine for 3 days with the first dose at 15 min before the surgery or intracerebroventricular injection of GDNF or an anti-GDNF antibody at the end of surgery. One week later, rats were started to be tested by Barnes maze and fear conditioning. Hippocampus was harvested at 6 h, 24 h or 10 days after the surgery for biochemical analysis. C8-B4 cells, a microglial cell line, were pretreated with 1 ng/ml GDNF for 30 min before being exposed to 5 ng/ml lipopolysaccharide for 2 h.Surgery increased the time to identify the target box in the Barnes maze when tested 1 day [22 (median) (11-66) (interquartile range) of control group vs. 158 (29-180) of surgery group, n = 15, P = 0.022) or 8 days after the training sessions and reduced context-related freezing behavior in the fear conditioning test. These effects were attenuated by amantadine (25 (14-90), n = 15, P = 0.029 compared with surgery group at 1 day after the training sessions in Barnes maze) and intracerebroventricular GDNF. Amantadine increased GDNF that was co-localized with glial fibrillary acidic protein, an astrocytic marker, in the hippocampus. Intracerebroventricular injection of an anti-GDNF antibody but not the denatured antibody blocked the effects of amantadine on cognition. Surgery induced neuroinflammation that was inhibited by amantadine. Lipopolysaccharide increased interleukin 1Î² production from C8-B4 cells. This effect was inhibited by GDNF.Our results suggest that amantadine attenuated surgery-induced learning and memory impairment. This effect may be mediated by GDNF via inhibition of neuroinflammation.
Critical role of inflammatory cytokines in impairing biochemical processes for learning and memory after surgery in rats. - Journal of neuroinflammation
Patients with postoperative cognitive dysfunction have poor outcomes. Neuroinflammation may be the underlying pathophysiology for this dysfunction. We determined whether proinflammatory cytokines affect the trafficking of Î±-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors to the plasma membrane, a fundamental biochemical process for learning and memory.Four-month-old male Fischer 344 rats were subjected to right carotid exposure under isoflurane anesthesia. Some rats received intravenous lidocaine infusion during anesthesia. Rats were tested two weeks later by Barnes maze. The hippocampus was harvested six hours after the surgery for western blotting of interleukin (IL)-1Î² or IL-6. Hippocampal slices were prepared from control rats or rats subjected to surgery two weeks previously. They were incubated with tetraethylammonium, an agent that can induce long term potentiation, for determining the trafficking of GluR1, an Î±-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor subunit.Surgery or anesthesia increased the time to identify the target box during the Barnes maze test training sessions and one day after the training sessions. Surgery also prolonged the time to identify the target box eight days after the training sessions. Surgery increased IL-1Î² and IL-6 in the hippocampus. The tetraethylammonium-induced GluR1 phosphorylation and trafficking were abolished in the hippocampal slices of rats after surgery. These surgical effects were partly inhibited by lidocaine. The incubation of control hippocampal slices with IL-1Î² and IL-6 abolished tetraethylammonium-induced GluR1 trafficking and phosphorylation. Lidocaine minimally affected the effects of IL-1Î² on GluR1 trafficking.Our results suggest that surgery increases proinflammatory cytokines that then inhibit GluR1 trafficking, leading to learning and memory impairment.
Long-term survival after resection of hepatocelluar carcinoma: a potential risk associated with the choice of postoperative analgesia. - Anesthesia and analgesia
Associations between anesthetic management and cancer recurrence or long-time survival remain uncertain. In this study, we compared the effects of postoperative epidural morphine analgesia with that of postoperative IV fentanyl analgesia on cancer recurrence and long-term survival in patients undergoing resection of hepatocellular carcinoma.A retrospective cohort study was performed on patients with hepatocellular carcinoma receiving hepatic resection at this institution (n = 1846, 1997-2007). Recurrence-free survival and long-term survival were assessed using Kaplan-Meier survival estimates and compared using a multivariate Cox proportional hazards regression, adjusted with propensity scores.Eight hundred nineteen patients met the inclusion criteria and were divided into 2 groups: patients receiving postoperative epidural analgesia with morphine (EA, n = 451) and patients receiving postoperative IV analgesia with fentanyl (IA, n = 368). The median time of follow-up for all patients was 4.2 years (2-9). The rates of recurrence of cancer (37.7% vs 30.7%, P = 0.036) and death (40.6% vs 30.4%, P = 0.003) were higher in the EA group versus IA group. Recurrence-free survival was similar in both the EA and IA groups (hazards ratio 2.224, 95% confidence interval, 0.207-23.893, P = 0.509). Using a multivariate Cox proportional hazards regression adjusted with propensity scores, independent risk factors for long-term survival in patients after resection of hepatocellular carcinoma were ASA physical status, tumor diameter, preoperative Î±-fetoprotein (+) as well as postoperative epidural analgesia with morphine.Compared with postoperative IV analgesia with fentanyl, postoperative epidural analgesia with morphine was associated with increased cancer recurrence and death but had no significant effect on recurrence-free survival in patients undergoing resection of hepatocellular carcinoma.
Glutamate transporter type 3 regulates mouse hippocampal GluR1 trafficking. - Biochimica et biophysica acta
Rapid trafficking of Î±-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) to the plasma membrane is considered a fundamental biological process for learning and memory. GluR1 is an AMPAR subunit. We have shown that mice with knockout of excitatory amino acid transporter type 3 (EAAT3), a neuronal glutamate transporter, have impaired learning and memory. The mechanisms for this impairment are not known and may be via regulation of AMPAR trafficking.Freshly prepared 300Î¼m coronal hippocampal slices from wild-type or EAAT3 knockout mice were incubated with or without 25mM tetraethylammonium for 10min. The trafficking of GluR1, an AMPAR subunit, to the plasma membrane and its phosphorylation were measured.Tetraethylammonium increased the trafficking of GluR1 and EAAT3 to the plasma membrane in the wild-type mouse hippocampal slices but did not cause GluR1 trafficking in the EAAT3 knockout mice. Tetraethylammonium also increased the phosphorylation of GluR1 at S845, a protein kinase A (PKA) site, in the wild-type mice but not in the EAAT3 knockout mice. The PKA antagonist KT5720 attenuated tetraethylammonium-induced GluR1 phosphorylation and trafficking in the wild-type mice. The PKA agonist 6-BNz-cAMP caused GluR1 trafficking to the plasma membrane in the EAAT3 knockout mice. In addition, EAAT3 was co-immunoprecipitated with PKA.These results suggest that EAAT3 is upstream of PKA in a pathway to regulate GluR1 trafficking.Our results provide initial evidence for the involvement of EAAT3 in the biochemical cascade of learning and memory.Copyright Â© 2014 Elsevier B.V. All rights reserved.
Electroacupuncture preconditioning-induced neuroprotection may be mediated by glutamate transporter type 2. - Neurochemistry international
Electroacupuncture has been shown to induce a preconditioning effect in the brain. The mechanisms for this protection are not fully elucidated. We hypothesize that this protection is mediated by excitatory amino acid transporters (EAATs) that have been shown to be neuroprotective. To test this hypothesis, two-month old male Sprague-Dawley rats and EAAT type 3 (EAAT3) knockout mice received or did not receive 30-min electroacupuncture once a day for five consecutive days. They were subjected to a 120-min middle cerebral arterial occlusion (MCAO) at 24h after the last electroacupuncture. Neurological outcome was assessed 2days after the MCAO. Brain tissues were harvested at 24h after the last electroacupuncture for Western blotting. Rats subjected to electroacupuncture at the Baihui acupoint had smaller brain infarct volumes and better neurological deficit scores than control rats. Electroacupuncture increased EAAT type 2 (EAAT2) in the cerebral cortex, tended to increase EAAT3 in the hippocampus, and had no effect on EAAT type 1 expression. Dihydrokainate, an EAAT2 inhibitor, worsened the neurological outcome of rats with electroacupuncture pretreatment. Electroacupuncture pretreatment at the Baihui acupoint increased EAAT2 in the cerebral cortex and improved the neurological outcome of EAAT3 knockout mice. Together, our results suggest that EAAT2 may mediate the electroacupuncture preconditioning-induced neuroprotection.Copyright Â© 2013 Elsevier Ltd. All rights reserved.
Surgical management of skull base chondroblastoma. - The Laryngoscope
Chondroblastoma is a rare tumor accounting for 1% of primary bone tumors. Chondroblastoma involving the skull base is exceedingly rare with approximately 60 cases reported. We reviewed our experience with chondroblastoma of the skull base with an emphasis on current lateral skull base approaches and long-term tumor control.A retrospective case review at a tertiary neurotology private practice group was performed over a 20-year period. Five patients were identified with skull base chondroblastoma. All patients underwent surgical intervention, and success of surgery was determined by disease-free status at last follow-up. Mean follow-up time was 5.8 years.Two patients underwent gross tumor removal as primary therapy. One patient underwent partial tumor removal at an outside institution, and follow-up magnetic resonance imaging demonstrated rapid growth of residual tumor. This patient was successfully treated with gross total removal of residual tumor with an infratemporal craniotomy approach. Near total tumor removal was performed in two patients because of intimate involvement of vital structures. At last follow-up, no patient had radiographic evidence of tumor recurrence. There were no significant postoperative complications.Gross total or near total resection of skull base chondroblastomas through lateral skull base approaches results in long-term tumor control and low complication rates.
Modeling notch signaling in normal and neoplastic hematopoiesis: global gene expression profiling in response to activated notch expression. - Stem cells (Dayton, Ohio)
In normal hematopoiesis, proliferation is tightly linked to differentiation in ways that involve cell-cell interaction with stromal elements in the bone marrow stem cell niche. Numerous in vitro and in vivo studies strongly support a role for Notch signaling in the regulation of stem cell renewal and hematopoiesis. Not surprisingly, mutations in the Notch gene have been linked to a number of types of malignancies. To better define the function of Notch in both normal and neoplastic hematopoiesis, a tetracycline-inducible system regulating expression of a ligand-independent, constitutively active form of Notch1 was introduced into murine E14Tg2a embryonic stem cells. During coculture, OP9 stromal cells induce the embryonic stem cells to differentiate first to hemangioblasts and subsequently to hematopoietic stem cells. Our studies indicate that activation of Notch signaling in flk+ hemangioblasts dramatically reduces their survival and proliferative capacity and lowers the levels of hematopoietic stem cell markers CD34 and c-Kit and the myeloid marker CD11b. Global gene expression profiling of day 8 hematopoietic progenitors in the absence and presence of activated Notch yield candidate genes required for normal hematopoietic differentiation, as well as putative downstream targets of oncogenic forms of Notch including the noncanonical Wnts Wnt4 and 5A. Disclosure of potential conflicts of interest is found at the end of this article.
Non-Invasive, Focal Disconnection of Brain Circuitry Using Magnetic Resonance-Guided Low-Intensity Focused UltrasoundÂ to Deliver a Neurotoxin. - Ultrasound in medicine & biology
Disturbances in the function of neuronal circuitry contribute to most neurologic disorders. As knowledge of the brain's connectome continues to improve, a more refined understanding of the role of specific circuits in pathologic states will also evolve. Tools capable of manipulating identified circuits in a targeted and restricted manner will be essential not only to expand our understanding of the functional roles of such circuits, but also to therapeutically disconnect critical pathways contributing to neurologic disease. This study took advantage of the ability of low-intensity focused ultrasound (FUS) to transiently disrupt the blood-brain barrier (BBB) to deliver a neurotoxin with poor BBB permeability (quinolinic acid [QA])Â in a guided manner to a target region in the brain parenchyma. Ten male Sprague-Dawley rats were divided into two groups receiving the following treatments: (i) magnetic resonance-guided FUSÂ +Â microbubblesÂ +Â saline (nÂ =Â 5), or (ii) magnetic resonance-guided FUSÂ +Â microbubblesÂ +Â QA (nÂ =Â 5). Systemic administration of QA was well tolerated. However, when QA and microbubbles were systemicallyÂ administered in conjunction with magnetic resonance-guided FUS, the BBB was disrupted and primary neurons were destroyed in the targeted subregion of the hippocampus in all QA-treated animals. Administration of vehicle (saline) together with microbubbles and FUS also disrupted the BBB but did not produce neuronal injury. These findings indicate the feasibility of non-invasively destroying a targeted region of the brain parenchyma using low-intensity FUS together with systemic administration of microbubbles and a neurotoxin. This approach could be of therapeutic value in various disorders in which disturbances of neural circuitry contribute to neurologic disease.Copyright Â© 2016 World Federation for Ultrasound in Medicine & Biology. Published by Elsevier Inc. All rights reserved.
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2131 W 3Rd St Los Angeles, CA 90057
2105 Beverly Blvd Suite 111
2023 Beverly Blvd
349 S La Fayette Park Pl Apt 104
520 S Lafayette Pk Pl 3Rd Floor
520 South Lafayette Pk. Pl. 3Rd Floor
2105 Beverly Blvd Ste 227