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Dr. David A Schweck  Md image

Dr. David A Schweck Md

15229 Us 31 N
Westfield IN 46074
317 671-1236
Medical School: Other - 2002
Accepts Medicare: Yes
Participates In eRX: Yes
Participates In PQRS: No
Participates In EHR: No
License #: 01061793
NPI: 1023045622
Taxonomy Codes:
207Q00000X

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Awards & Recognitions

About Us

Practice Philosophy

Conditions

Dr. David A Schweck is associated with these group practices

Procedure Pricing

HCPCS Code Description Average Price Average Price
Allowed By Medicare
HCPCS Code:99214 Description:Office/outpatient visit est Average Price:$139.00 Average Price Allowed
By Medicare:
$99.01
HCPCS Code:99213 Description:Office/outpatient visit est Average Price:$94.00 Average Price Allowed
By Medicare:
$66.84
HCPCS Code:G0328 Description:Fecal blood scrn immunoassay Average Price:$32.00 Average Price Allowed
By Medicare:
$22.53
HCPCS Code:81003 Description:Urinalysis auto w/o scope Average Price:$10.00 Average Price Allowed
By Medicare:
$3.18
HCPCS Code:81002 Description:Urinalysis nonauto w/o scope Average Price:$7.00 Average Price Allowed
By Medicare:
$3.62

HCPCS Code Definitions

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.
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.
G0328
Colorectal cancer screening; fecal occult blood test, immunoassay, 1-3 simultaneous

Medical Malpractice Cases

None Found

Medical Board Sanctions

None Found

Referrals

None Found

Publications

Menin promotes the Wnt signaling pathway in pancreatic endocrine cells. - Molecular cancer research : MCR
Menin is a tumor suppressor protein mutated in patients with multiple endocrine neoplasia type 1. We show that menin is essential for canonical Wnt/beta-catenin signaling in cultured rodent islet tumor cells. In these cells, overexpression of menin significantly enhances TCF gene assay reporter activity in response to beta-catenin activation. Contrastingly, inhibition of menin expression with Men1 siRNA decreases TCF reporter gene activity. Likewise, multiple endocrine neoplasia type 1 disease associated missense mutations of menin abrogate the ability to increase TCF reporter gene activity. We show that menin physically interacts with proteins involved in the canonical Wnt signaling pathway, including beta-catenin, TCF3 (TCFL1), and weakly with TCF4 (TCFL2). Menin overexpression increases expression of the Wnt/beta-catenin downstream target gene Axin2, which is associated with increased H3K4 trimethylation of the Axin2 gene promoter. Moreover, inhibition of menin expression by siRNA abrogates H3K4 trimethylation and Axin2 gene expression. Based on these studies, we hypothesized that Wnt signaling could inhibit islet cell proliferation because loss of menin function is thought to increase endocrine tumor cell proliferation. TGP61 rodent islet tumor cells treated with a glycogen synthase kinase 3beta inhibitor that increases Wnt pathway signaling had decreased cell proliferation compared with vehicle-treated cells. Collectively, these data suggest that menin has an essential role in Wnt/beta-catenin signaling through a mechanism that eventually affects histone trimethylation of the downstream target gene Axin2, and activation of Wnt/beta-catenin signaling inhibits islet tumor cell proliferation.

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15229 Us 31 N Westfield, IN 46074
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