Dr. Robert  Finlay  Od image

Dr. Robert Finlay Od

6530 Farmington Rd Ste 300
West Bloomfield MI 48322
248 615-5100
Medical School: Other - Unknown
Accepts Medicare: No
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: No
License #: L445954
NPI: 1730104803
Taxonomy Codes:

Request Appointment Information

Awards & Recognitions

About Us

Practice Philosophy


Medical Malpractice Cases

None Found

Medical Board Sanctions

None Found


None Found


Smooth muscle protein-22-mediated deletion of Tsc1 results in cardiac hypertrophy that is mTORC1-mediated and reversed by rapamycin. - Human molecular genetics
Constitutive activation of mammalian target of rapamycin complex 1 (mTORC1), a key kinase complex that regulates cell size and growth, is observed with inactivating mutations of either of the tuberous sclerosis complex (TSC) genes, Tsc1 and Tsc2. Tsc1 and Tsc2 are highly expressed in cardiovascular tissue but their functional role there is unknown. We generated a tissue-specific knock-out of Tsc1, using a conditional allele of Tsc1 and a cre recombinase allele regulated by the smooth muscle protein-22 (SM22) promoter (Tsc1c/cSM22cre+/-) to constitutively activate mTOR in cardiovascular tissue. Significant gene recombination (∼80%) occurred in the heart by embryonic day (E) 15, and reduction in Tsc1 expression with increased levels of phosphorylated S6 kinase (S6K) and S6 was observed, consistent with constitutive activation of mTORC1. Cardiac hypertrophy was evident by E15 with post-natal progression to heart weights of 142 ± 24 mg in Tsc1c/cSM22cre+/- mice versus 65 ± 14 mg in controls (P < 0.01). Median survival of Tsc1c/cSM22cre+/- mice was 24 days, with none surviving beyond 6 weeks. Pathologic and echocardiographic analysis revealed severe biventricular hypertrophy without evidence of fibrosis or myocyte disarray, and significant reduction in the left ventricular end-diastolic diameter (P < 0.001) and fractional index (P < 0.001). Inhibition of mTORC1 by rapamycin resulted in prolonged survival of Tsc1c/cSM22cre+/- mice, with regression of ventricular hypertrophy. These data support a critical role for the Tsc1/Tsc2-mTORC1-S6K axis in the normal development of cardiovascular tissue and also suggest possible therapeutic potential of rapamycin in cardiac disorders where pathologic mTORC1 activation occurs.
Production and characterization of a monoclonal antibody against mannose-sensitive hemagglutinin of Vibrio cholerae. - Hybridoma
We have generated murine monoclonal antibodies (MAb) against Vibrio cholerae mannose-sensitive hemagglutinin (MSHA) using conventional hybridoma procedures. Seven hybridomas were obtained and one characterized. Hybridoma 2F12/F1 secreted an antibody of the IgG3 type that reacted with a 17-kDa antigen corresponding to the product of the mshA gene. This MAb inhibited mannose-sensitive agglutination of chicken erythrocytes by EL tor and O139 vibrios. Vibrios expressing MSHA activity inhibited binding of the antibody secreted by 2F12/F1 to MSHA-coated microtiter plates.

Map & Directions

6530 Farmington Rd Ste 300 West Bloomfield, MI 48322
View Directions In Google Maps

Nearby Doctors

6777 W Maple Rd
West Bloomfield, MI 48322
843 768-8023
6400 Farmington Road
West Bloomfield, MI 48322
248 614-4000
6621 W Maple Rd
W Bloomfield, MI 48322
248 614-4700
6555 W Maple Rd
West Bloomfield, MI 48322
248 922-2654
5829 W Maple Rd Suite 123
West Bloomfield, MI 48322
248 378-8066
5111 Cedarhurst Dr
West Bloomfield, MI 48322
248 702-2348
6555 W Maple Rd
West Bloomfield, MI 48322
248 922-2300
7296 Simsbury Dr
West Bloomfield, MI 48322
248 372-2343
5665 W Maple #A
West Bloomfield, MI 48322
248 268-8884
5665 W Maple Rd Suite A
West Bloomfield, MI 48322
248 268-8833