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Uma Yallampalli

Researcher at Baylor College of Medicine

Publications -  33
Citations -  781

Uma Yallampalli is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: Pregnancy & Placenta. The author has an hindex of 16, co-authored 33 publications receiving 710 citations. Previous affiliations of Uma Yallampalli include University of Texas Medical Branch & Boston Children's Hospital.

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Proliferation and differentiation of a human colon cancer cell line (CaCo2) is associated with significant changes in the expression and secretion of insulin-like growth factor (IGF) IGF-II and IGF binding protein-4: role of IGF-II.

TL;DR: The studies suggest that differential expression of IGF-II and IGFBPs may be playing a critical role in both proliferation and differentiation of colonocytes, and suggested that CaCo2 cell differentiation may require an attenuation ofIGF-II effects.
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Protein restriction during pregnancy induces hypertension and impairs endothelium-dependent vascular function in adult female offspring

TL;DR: The decreasedNO-mediated vascular response might explain the increased vascular contraction and arterial pressure infemale offspring with low birth weight.
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Fetal programming of adult hypertension in female rat offspring exposed to androgens in utero

TL;DR: Elevated plasma maternal testosterone levels causes low birth weight followed by catch-up growth and hypertension in female offspring and alters endothelium-dependent vascular responses.
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Injection of adjuvant but not acidic saline into craniofacial muscle evokes nociceptive behaviors and neuropeptide expression.

TL;DR: These findings extend earlier reports that CFA-induced muscle inflammation results in behavioral and neuropeptide changes and imply that disparate proton sensing mechanisms underlie these discrepancies in craniofacial muscle pain.
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Muscle inflammation induces a rapid increase in calcitonin gene-related peptide (CGRP) mRNA that temporally relates to CGRP immunoreactivity and nociceptive behavior.

TL;DR: The hypothesis that CGRP is upregulated during deep tissue inflammation is supported and the suggestion that gene transcription is involved in this upregulation is suggested.