Bruce A. Boston

ORCID: 0000-0001-9808-2275
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About
Contact & Profiles
Research Areas
  • Regulation of Appetite and Obesity
  • Biochemical Analysis and Sensing Techniques
  • melanin and skin pigmentation
  • Adipokines, Inflammation, and Metabolic Diseases
  • Growth Hormone and Insulin-like Growth Factors
  • Sexual Differentiation and Disorders
  • Adrenal Hormones and Disorders
  • Bone health and osteoporosis research
  • Metabolism and Genetic Disorders
  • Thyroid Disorders and Treatments
  • Diet and metabolism studies
  • Hypothalamic control of reproductive hormones
  • Neuroblastoma Research and Treatments
  • Hormonal Regulation and Hypertension
  • Bone Tumor Diagnosis and Treatments
  • Obesity, Physical Activity, Diet
  • Neonatal Health and Biochemistry
  • Adipose Tissue and Metabolism
  • Craniofacial Disorders and Treatments
  • Cleft Lip and Palate Research
  • Electrolyte and hormonal disorders
  • Medication Adherence and Compliance
  • Dye analysis and toxicity
  • TGF-β signaling in diseases
  • Diabetes Management and Research

Oregon Health & Science University
2004-2020

Doernbecher Children's Hospital
2011-2014

Columbia University
2000

Vollum Institute
1997-1998

Millennium Engineering and Integration (United States)
1998

Merck & Co., Inc., Rahway, NJ, USA (United States)
1997

Oregon State Hospital
1993

University of Ulster
1992

Royal Belfast Hospital for Sick Children
1992

Queens University
1992

The lethal yellow ( A Y /a ) mouse has a defect in proopiomelanocortin (POMC) signaling the brain that leads to obesity, and is resistant anorexigenic effects of hormone leptin. It been proposed weight-reducing leptin are thus transmitted primarily by way POMC neurons. However, central defective signaling, absence leptin, on weight gain double-mutant leptin-deficient lep ob /lep mice were shown be independent additive. Furthermore, deletion gene restored sensitivity mice. This result implies...

10.1126/science.278.5343.1641 article EN Science 1997-11-28

It has been known for many years that adipocytes express high affinity ACTH and alpha-melanocyte stimulating hormone (MSH) binding sites, ACTH, alpha-MSH, beta-lipotropin are potent lipolytic hormones. We show here the adipocyte response to melanocortin peptides results from expression of both MC2 (ACTH) receptor as well newly discovered MC5 receptor. Using RT-PCR Northern blot hybridization, levels messenger RNA (mRNA) were found in all adipose tissues examined mouse, whereas mRNA was a...

10.1210/endo.137.5.8612546 article EN Endocrinology 1996-05-01

It has been known for many years that adipocytes express high affinity ACTH and alpha-melanocyte stimulating hormone (MSH) binding sites, ACTH, alpha-MSH, beta-lipotropin are potent lipolytic hormones. We show here the adipocyte response to melanocortin peptides results from expression of both MC2 (ACTH) receptor as well newly discovered MC5 receptor. Using RT-PCR Northern blot hybridization, levels messenger RNA (mRNA) were found in all adipose tissues examined mouse, whereas mRNA was a...

10.1210/en.137.5.2043 article EN Endocrinology 1996-05-01

Abstract Background Imatinib mesylate, a tyrosine kinase inhibitor, is used in the treatment of chronic myelogeneous leukemia (CML). Given its ease administration and manageable side effects adults, imatinib mesylate was introduced as therapy for pediatric CML. Recently published case reports describe growth deceleration children treated with imatinib. This study details phenotype seven patients maintained remission on imatnib over an extended period time. Procedure retrospective chart...

10.1002/pbc.24121 article EN Pediatric Blood & Cancer 2012-02-29

The mahogany ( mg ) locus originally was identified as a recessive suppressor of agouti , encoding skin peptide that modifies coat color by antagonizing the melanocyte-stimulating hormone receptor or MC1-R. Certain dominant alleles cause an obesity syndrome when ectopic expression aberrantly antagonizes MC4-R, related expressed in hypothalamic circuitry and involved regulation feeding behavior metabolism. Recent work has demonstrated homozygous, blocks not only ability to induce yellow...

10.1073/pnas.95.21.12707 article EN Proceedings of the National Academy of Sciences 1998-10-13

Cushing's syndrome in infancy is uncommon. In this report, we describe an infant with ACTH-independent which activating mutation the stimulatory G-protein (Gs alpha) was detected. The patient presented at 3 months of age Cushingoid features, poor linear growth, and elevated liver enzymes. Plasma ACTH dexamethasone suppression test results were consistent syndrome, a subsequent adrenalectomy revealed bilateral adrenocorticonodular hyperplasia. Asymptomatic lesions fibrous dysplasia later...

10.1210/jcem.79.3.8077378 article EN The Journal of Clinical Endocrinology & Metabolism 1994-09-01

Height velocity (HV) is difficult to assess because growth very slow. The current practice of calculating it from measurements taken at several-month intervals insufficient for managing children with disorders. We identified a bone by-product (collagen X biomarker, CXM) in blood that preliminary analysis healthy correlated strongly conventionally determined HV and displayed pattern resembling published norms vs age.

10.1210/clinem/dgaa721 article EN cc-by The Journal of Clinical Endocrinology & Metabolism 2020-10-09

Introduction:We reviewed the impact of telehealth videoconferencing clinics on outcomes care in pediatric patients with type 1 diabetes rural Oregon. Methods:We performed a chart review as well patient satisfaction questionnaires from 27 seen first year program. Results:The number yearly visits to clinic increased average 1.5 2.7, which was statistically significant (p < 0.0001). Glycemic control remained stable, and there no difference amount emergency department or hospitalizations related...

10.1089/tmj.2017.0072 article EN Telemedicine Journal and e-Health 2017-06-27

Article A Novel Presentation of Familial Glucocorticoid Deficiency (FGD) and Current Literature Review was published on January 1, 2004 in the journal Journal Pediatric Endocrinology Metabolism (volume 17, issue 1).

10.1515/jpem.2004.17.1.85 article EN Journal of Pediatric Endocrinology and Metabolism 2004-01-01
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