Biomedical subjects

Tam N Pham

Publications and source records attributed to Tam N Pham.

8 recordsLinked to original sources

PubMed2007

Thermal and electrical injuries.

Through progress in wound management, resuscitation, intensive care treatment, and a coordinated rehabilitation process, modern burn care has been able to deliver substantial increases in survival and improvement in functional outcomes for burn victims. The development of regionalized burn centers has contributed greatly to this progress. As the field of burns matures, burn centers are preparing to meet future challenges through collaborative efforts in disaster management and outcomes research.

Anemia↗

PubMed2005

CD14-dependent modulation of transcriptional activities of endogenous retroviruses in the lung after injury.

Lipopolysaccharide (LPS) plays a central role in the pathogenesis of distant organs after burn. Recent studies demonstrated the regulation of mouse endogenous retroviruses (MuERVs) in several organs after burn. In this study, the role of CD14, a LPS receptor, in burn-mediated regulation of MuERV expression in the lung was investigated. CD14 knockout (KO) and wild type (WT) mice were subjected to burn followed by RT-PCR analysis of alterations in the MuERV expression in the lung 1 day after injury. Even without injury, CD14 KO mice had a unique profile of MuERV expression compared to WT. Three bands (Lung-1, Lung-2, and Lung-3) in CD14 KO were downregulated after injury. Lung-2 and Lung-3 transcripts were almost identical to 2 previously described defective env transcripts of MuERVs, respectively. The Lung-1-1 transcript was a double spliced message generated by the env and a set of novel splicing signals, whereas the Lung-1-2 transcript was a defective env transcript. Only the Lung-1-1 transcript had a significant ORF capable of encoding a gag-pol fusion polypeptide. Putative proviral sequences of Lung-1-1 and Lung-1-2 transcripts were mapped to chromosomes 4 and 11, respectively. The results from this study suggest that the absence of CD14 expression in CD14 KO mice contributes to the transcriptional regulation of MuERVs in the lung after injury.

Animals↗

PubMed2005

Impact of tight glycemic control in severely burned children.

BACKGROUND: Control of hyperglycemia has been shown to decrease mortality in critically ill adults, but the benefits of strict glucose control have not been established in children. Since January 2002, our pediatric burn center has adopted a policy of 'intensive' insulin therapy to achieve blood glucose levels 90 to 120 mg/dL. The purpose of this study was to examine the impact of this practice on patient outcomes. METHODS: We reviewed the records of children with > or =30% total body surface area (TBSA) burn injury admitted to our regional pediatric burn center from July 1, 2000 to June 31, 2003. Patients were grouped into 'conventional insulin therapy' for the 2000 to 2001 period (n = 31) and into 'intensive insulin therapy' for the 2002 to 2003 period (n = 33). The efficacy of glucose control, infection rates, and patient survival were compared for the two therapies. RESULTS: The demographic characteristics and injury severity were similar between the conventional and intensive insulin therapy groups. Children receiving intensive insulin therapy had glucose levels of 90 to 120 mg/dL more consistently than those in the conventional insulin therapy group. There was a significant decrease in urinary tract infections among intensive insulin therapy patients. TBSA burn, percent full-thickness burn, and Pediatric Risk of Mortality scores were negatively related to survival; intensive insulin therapy was positively associated with survival. CONCLUSION: Intensive insulin therapy to maintain normoglycemia in severely burned children can be safely and effectively implemented in the burn unit. This therapy seems to lower infection rates and improve survival. Intensive insulin therapy should be considered for children with severe burn injuries.

Blood Glucose↗

PubMed2004

Involvement of CD14 and toll-like receptor 4 in the acute phase response of serum amyloid A proteins and serum amyloid P component in the liver after burn injury.

Acute phase proteins such as serum amyloid A proteins (SAAs) and serum amyloid P component (SAP) are induced in the liver after various insults (e.g., infection, injury). The cellular and molecular mechanisms controlling the expression of these acute phase proteins may be specifically designed for different insults. The roles of two central molecules of the lipopolysaccharide (LPS)-mediated inflammation pathway (CD14 and toll-like receptor 4 [Tlr4]) were investigated for the regulation of SAAs and SAP in the liver of mice after an 18% total body surface area burn injury. RT-PCR analysis revealed a subtype- and time-dependent induction of SAA mRNAs between 3 h and 3 days, while there was a peak induction of SAP mRNA at day 1. Marked elevations of SAA and SAP protein levels at day 1 supported the mRNA data. Furthermore, a differential regulation of SAAs and SAP mRNAs was noted between CD14 knockout (KO) and their control mice after injury. SAA protein was induced to a lesser degree after injury in C3H/HeJ (Tlr4-defective) mice than in their control mice. In addition, in both CD14 KO and C3H/HeJ mice, the induction of SAP protein was significantly reduced compared with respective controls. These data provide evidence that CD14 and Tlr4 participate, at least in part, in a cascade of signaling events that control the immediate-early and differential induction of SAAs and SAP in the liver after injury. They also suggest that LPS may be one of the initial inducing agents associated with these acute phase responses in the liver after injury.

Acute-Phase Reaction↗

PubMed2004

Reduced hepatic expression of glutathione s-transferases in burned mice.

BACKGROUND: Glutathione S-transferases (GSTs) contribute to liver homeostasis and are released into plasma after liver injury. This study investigates the hepatic expression of key GST enzyme subtypes after burn injury. METHODS: Mice were subjected to an 18% total body surface area burn. Expression of mGSTalpha3 and mGSTmu1 was analyzed by reverse-transcriptase polymerase chain reaction and Western blots on liver preparations from burned and control mice. GST catalytic activity was measured by conjugation assays. RESULTS: : In burned animals, mGSTalpha3 mRNA was only reduced at 1 day, whereas mGSTmu1 mRNA decreased at 1 day and at 3 days after injury. Total mGSTmu protein levels decreased at the same time points, whereas total mGSTalpha protein levels did not change. Also, by 3 days, total GST conjugation activity was reduced by 25% (p=0.05). CONCLUSION: Reduced expression of specific alpha and mu GST enzymes after burns correlates functionally with reduced GST activity. Altered GST expression may contribute to liver damage after systemic injury.

Animals↗

PubMedDate not supplied

Burn injury induces an inhibitory signal in the lung Smad pathway.

Smad signaling mediates the cellular response to transforming growth factor-beta (TGF-beta). We hypothesize that variations in Smad signaling modify the response to TGF-beta signaling in the lung after injury. C57BLKS/J mice were subjected to an 18% surface area burn injury, sacrificed at specific time points and their lung tissue was harvested. Lung TGF-beta1 expression, as determined by RT-PCR, ELISA and PAI/Luciferase assay, was not affected by injury. Western blots for Smad2/3 and Smad4 on nuclear fractions revealed decreased Smad2, Smad3, and Smad4 protein levels at 3h, while their total cellular levels did not differ from control mice. Smad7 protein increased transiently at 3 h. Correlating with Smad inhibition, transcription in type I alpha-2 collagen was also transiently depressed. By RT-PCR, Smad3 and Smad7 mRNAs decreased at 3 h, while Smad2 and Smad4 mRNA levels remained constitutive. Burn injury did not alter lung TGF-beta1 expression but caused Smad inhibition through decreased nuclear translocation of Smad2, Smad3, and Smad4, and upregulated Smad7. Transcription was not the key regulatory step in Smad protein expression, as transient decreases in Smad3 and Smad7 mRNA did not correlate with protein levels. It appears that Smad activity may in part attenuate TGF-beta activity after burn injury.

Animals↗

PubMedDate not supplied

Predisposing factors for self-inflicted burns.

Self-inflicted burn injuries, although uncommon, are a significant source of morbidity and mortality. The purpose of this study was to delineate the characteristics of these burns and to examine their impact on society. Records of 32 adult patients admitted for self-inflicted burns at our regional burn center between January 1996 and August 2001 were retrospectively reviewed. The mean burn size was 34 +/- 29% TBSA, with the majority of burns being the result of self-immolation using a flammable liquid. There was a slight male predominance (59%) and a significant mortality rate (25%). Ninety-one percent of patients had an active psychiatric diagnosis, with 47% having had a previous suicide attempt. Two thirds had a chronic stressor, such as a chronic medical illness and/or long-term disability. Only four patients had private insurance, whereas the remainder relied on underfunded state- and county-sponsored programs or were uninsured. In addition to well-described psychiatric factors, common characteristics predisposing to self-inflicted burns include chronic medical illnesses, long-term disability, and a lack of access to adequate mental health care. Better treatment of mental illness in the underfunded population might ultimately save the high costs of these burn injuries.

Adolescent↗

PubMedDate not supplied

The clinical pulmonary infection score poorly predicts pneumonia in patients with burns.

The Clinical Pulmonary Infection Score (CPIS) has been reported to be a useful tool in the diagnosis of ventilator-associated pneumonia (VAP) in the critical care setting. However, the systemic inflammation associated with injury may limit the utility of CPIS in patients with burns. The purpose of this study was to determine the potential utility of CPIS in the management of burn patients. A retrospective review was performed on all burn patients who underwent quantitative culture to diagnose VAP from 2003 to 2005. CPIS was retrospectively calculated for each patient on the day of the procedure. The sensitivity, specificity, and predictive values of a CPIS greater than 6 for VAP diagnosis were calculated. In addition, CPIS scores of patients with and without pneumonia were compared using the Mann-Whitney U test. A total of 46 quantitative cultures were obtained in 28 patients during the study period. Average patient age was 45 +/- 19 years, average TBSA was 33 +/- 18%, and the average APACHE II score on admission was 16 +/- 6. Sixty-eight percent of patients had inhalation injury. Twenty-six quantitative cultures were positive, and 20 were negative. Mean CPIS was 5.7 for patients with negative quantitative cultures and 5.5 for patients with positive cultures (P = .41). The sensitivity of CPIS scoring was 0.3, and its specificity was 0.8. CPIS had a positive predictive value of 0.7 and negative predictive value of 0.5. CPIS--a reported reliable indicator of VAP in critically ill patients--did not accurately predict the presence of pneumonia in burn patients. VAP diagnosis in burn patients should still rely on clinical suspicion verified by quantitative culture.

Adolescent↗