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Dr. Macy Ng Dc

2495 Old Middlefield Way
Mountain View CA 94043
650 698-8581
Medical School: Other - Unknown
Accepts Medicare: No
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: No
License #: 32486
NPI: 1023351046
Taxonomy Codes:
111N00000X

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Publications

Immunodiagnostic capabilities of anti-free immunoglobulin light chain monoclonal antibodies. - American journal of clinical pathology
Overproduction of plasma cell-derived monoclonal free kappa or lambda immunoglobulin light chains (FLCs) is a hallmark of multiple myeloma, AL amyloidosis, and light chain deposition disease. Because these components serve as unique cellular and serologic biomarkers, their detection and quantitation has diagnostic, therapeutic, and prognostic import. In this regard, we have developed monoclonal antibodies (mAbs) that specifically recognize the kappa or lambda FLC products of all known human variable and constant region light chain genes. We now report the results of our studies that have demonstrated the capability of these reagents to measure, in a modified fluid-phase capture enzyme-linked immunosorbent assay (ELISA), serum kappa and lambda FLCs at concentrations as low as 5 and 15 ng/mL, respectively. The mAb-based ELISA has greater sensitivity and reproducibility than does the commercially available immunoturbidimetric assay that uses polyclonal anti-FLC antibodies. In addition, the mAbs can immunostain monoclonal FLC-producing plasma cells and pathologic light chain-related amyloid and nonfibrillar tissue deposits. Our anti-FLC mAbs, with their high degree of reactivity and versatility, may provide an invaluable tool in the diagnosis and management of light chain-associated disease.
Association of sex hormones and adiposity with plasma levels of fibrinogen and PAI-1 in postmenopausal women. - American journal of epidemiology
Blood levels of the clotting factor fibrinogen and tissue plasminogen activator inhibitor-1 (PAI-1), a primary inhibitor of fibrinolysis, have been positively linked to risk of coronary heart disease. The authors have reported previously that plasma fibrinogen appears to rise after menopause and to be reduced with use of postmenopausal hormonal therapy. There is also evidence to suggest that sex hormones may influence PAI-1. To examine whether plasma fibrinogen and PAI-1 antigen levels differ among older postmenopausal women according to use of hormone therapy and by blood level of estrogen and androgens, these variables were assessed among 277 healthy women aged 65-82 years, one half of whom were receiving therapy. The study population was drawn from the Study of Osteoporotic Fractures, Pittsburgh, Pennsylvania, during 1986-1988. Overall, results showed median PAI-1 levels to be lower on average with oral and transdermal use of hormone therapy (25.0 vs. 33.5 ng/ml, p < 0.01) and mean fibrinogen levels to be lower (279 vs. 295 mg/dl, p < 0.02) with use of oral estrogen (but not transdermal) therapy compared with women not receiving therapy. Among women not receiving therapy, PAI-1 and fibrinogen levels were not related to endogenous sex hormone levels, with the exception of a modest positive relation between PAI-1 and serum estrone concentrations (rs = 0.29). In addition, a markedly higher PAI-1 level was found for women with a preponderance of upper body fat, independent of obesity. In sum, results showed that older women receiving postmenopausal hormone therapy had more favorable plasma levels of the hemostatic factors PAI-1 and fibrinogen than did those not receiving therapy, which can be explained in large part by differences between the two groups in obesity and body fat distribution.
Correlation between baseline plasminogen activator inhibitor levels and clinical outcome during therapy with tissue plasminogen activator for acute myocardial infarction. - Thrombosis and haemostasis
Baseline plasminogen activator inhibitor (PAI) levels were examined for their influence on the responses to thrombolysis with recombinant tissue plasminogen activator (rt-PA) administered for acute myocardial infarction during the Thrombolysis and Myocardial Infarction (TAMI)-I study. Baseline PAI activity was 19 +/- 21 IU/ml (normal less than 5 IU/ml) and baseline PAI-1 antigen 54 +/- 53 ng/ml (normal 27 +/- 16 ng/ml), confirming previous findings of elevated PAI levels during acute myocardial infarction. Among clinical outcomes, lower PAI-1 antigen levels correlated weakly with greater patency at the 90 min angiogram. Thus, high baseline plasma PAI-1 levels may be detrimental to reperfusion with t-PA. There was no correlation with other major in-hospital clinical outcomes including reocclusion at the 7-10 day angiogram, survival to discharge, or bleeding. During the follow up period of 2.0 +/- 0.4 years, no relationship between baseline PAI levels and post-discharge reinfarction was observed.
Effect of ophthalmic prednisolone acetate on the canine adrenal gland and hepatic function. - American journal of veterinary research
Iatrogenic hypothalamic-hypophysis-adrenal axis suppression occurred in 5 small dogs as a result of ophthalmic instillation of 1% prednisolone acetate. An ophthalmic suspension was applied 4 times a day to each eye, such that 4 mg/day was delivered for 2 weeks followed by 2.67 mg/day for 2 weeks. After treatment week 2, serum cortisol decreased from base-line mean values of 17.66 ng/ml (before ACTH) and 139.16 ng/ml (60 minutes after ACTH) to 3.22 ng/ml (before ACTH) and 13.58 ng/ml (60 minutes after ACTH). After treatment week 4, serum cortisol values decreased to a mean of 1.76 ng/ml (before ACTH) and 4.82 ng/ml (60 minutes after ACTH). Before ACTH cortisol values returned to base line 2 weeks after discontinuing treatment. Values after ACTH administration remained 26% lower than base line (P = 0.0132), although within a normal response range. Hepatic carbohydrate metabolism was altered, allowing marked glycogen accumulation. Marked increases in the blood glucose values after glucagon stimulation testing occurred at 3, 5, 15, 30, and 60 minutes after glucagon administration. The greatest increase corresponded to the 30-minute sample with a mean glucose increase of 112.40 mg/dl from base-line values (P = 0.0022) as a result of the ophthalmic corticosteroid applied. Seemingly, topical ophthalmic corticosteroids have the potential for causing adrenocortical suppression and hepatic metabolic changes. The dosage level of treatment was low enough to avoid major hematologic changes. The exaggerated response to the glucagon tolerance test indicates that this test can be used in detecting hyperglucocorticism.

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2495 Old Middlefield Way Mountain View, CA 94043
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