Publications by authors named "Douglas Y Tamura"

3 Publications

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Obesity Protects Against Operation in Pediatric Penetrating Trauma to the Torso.

J Surg Res 2021 Feb 24;263:57-62. Epub 2021 Feb 24.

Division of Pediatric Surgery, Valley Children's Hospital, Madera, California.

Background: Studies in the adult population are conflicting regarding whether obesity is protective in penetrating trauma. In the pediatric population, data on obesity and penetrating trauma are limited. We sought to determine if there is a different rate of operation or of survival in pediatric and adolescent patients with obesity.

Methods: We queried the National Trauma Data Bank research data set from 2013 to 2016 for all patients aged 2-18 who sustained traumatic penetrating injuries to the thorax and abdomen. The cohort was divided into body mass index percentiles for gender and age using Center for Disease Control definitions. Outcomes included overall survival, whether or not an operative procedure was performed, and hospital and intensive care unit (ICU) length of stay.

Results: We analyzed 9611 patients with penetrating trauma, of which 4285 had an operative intervention. When adjusted for other variables (age, gender, race, ICU length of stay, hospital length of stay, and Injury Severity Score), children of every body mass index percentile had similar survival. Healthy weight patients were more likely to get an operation than patients in the obese category. Length of hospital stay was similar between groups, but the ICU length of stay was longer in the overweight and obese groups compared with healthy weight and underweight groups.

Conclusions: Children and adolescents with obesity are less likely to undergo operation after penetrating thoracoabdominal trauma. Further study is needed to determine the reason for this difference.
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http://dx.doi.org/10.1016/j.jss.2021.01.021DOI Listing
February 2021

Fidget Spinner Battery-LED Unit Ingestion in a 13-Month-Old Boy.

Clin Pediatr (Phila) 2018 06 22;57(7):857-860. Epub 2017 Sep 22.

2 Valley Children's Hospital, Madera, CA, USA.

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http://dx.doi.org/10.1177/0009922817733302DOI Listing
June 2018

Acute hypoxemia in humans enhances the neutrophil inflammatory response.

Shock 2002 Apr;17(4):269-73

Department of Surgery, Denver Health Medical Center, Colorado, USA.

The neutrophil (PMN) is regarded as a key component in the hyperinflammatory response known as the systemic inflammatory response syndrome. Acute respiratory distress syndrome (ARDS) and subsequent multiple organ failure (MOF) are related to the severity of this hyperinflammation. ICU patients who are at highest risk of developing MOF may have acute hypoxic events that complicate their hospital course. This study was undertaken to evaluate the effects of acute hypoxia and subsequent hypoxemia on circulating PMNs in human volunteers. Healthy subjects were exposed to a changing O2/N2 mixture until their O2 saturation (SaO2) reached a level of 68% saturation. These subjects were then exposed to room air and then returned to their baseline SaO2. PMNs were isolated from pre- and post-hypoxemic arterial blood samples and were then either stimulated with N-formyl-methionyl-leucyl-phenylalanine (fMLP) or PMA alone, or they were primed with L-alpha-phosphatidylcholine, beta-acetyl-gamma-O-alkyl (PAF) followed by fMLP activation. Reactive oxygen species generation as measured by superoxide anion production was enhanced in primed PMNs after hypoxemia. Protease degranulation as measured by elastase release was enhanced in both quiescent PMNs and primed PMNs after fMLP activation following the hypoxemic event. Adhesion molecule upregulation as measured by CD11b/CD18, however, was not significantly changed after hypoxemia. Apoptosis of quiescent PMNs was delayed after the hypoxemic event. TNFalpha, IL-1, IL-6, and IL-8 cytokine levels were unchanged following hypoxemia. These results indicate that relevant acute hypoxemic events observed in the clinical setting enhance several PMN cytotoxic functions and suggest that a transient hypoxemic insult may promote hyperinflammation.
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http://dx.doi.org/10.1097/00024382-200204000-00005DOI Listing
April 2002