Annals of clinical and laboratory science
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Ann. Clin. Lab. Sci. · Jan 2008
Non-anion gap acidosis in asthma: clinical and laboratory features and outcomes for hospitalized patients.
Metabolic acidosis secondary to lactic acidosis may occur in acute, severe asthma and its presence suggests that respiratory muscle fatigue and tissue hypoxia play a major part in the pathogenesis. Non-anion gap metabolic acidosis (NAG acidosis) has also been reported in acute asthma but its impact on the clinical outcome has not been evaluated. The objective of this study was to evaluate the prevalence of NAG acidosis, characterize the laboratory findings, and determine its impact on clinical outcomes. ⋯ NAG acidosis was associated with a statistically significant (p = 0.028) risk of requirement for mechanical ventilation necessitating admission to the Medical Intensive Care Unit (MICU); the odds ratio for intubation for NAG acidosis compared to other groups was 3.92. No difference, however, was detected in overall length of stay (LOS) in hospital for patients with NAG acidosis vs the other groups. NAG metabolic acidosis in acute asthma may be more prevalent than expected and may be associated with more frequent need for mechanical ventilation and admission to an intensive care unit.
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Ann. Clin. Lab. Sci. · Jan 2008
Case ReportsKidney injury molecule-1 expression identifies proximal tubular injury in urate nephropathy.
Urate nephropathy in children is uncommon, occurring mostly in those who have undergone chemotherapy or radiotherapy. The characteristic obstruction of distal nephron tubules by uric acid precipitates is considered key to the subsequent parenchymal injury. ⋯ In their renal biopsies, we demonstrate upregulation of kidney injury molecule-1 (KIM-1), a specific injury marker, in proximal tubular cells. This finding implicates a role for proximal tubular injury in urate nephropathy.
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Ann. Clin. Lab. Sci. · Jan 2008
Influence of Nrf2 genotype on pulmonary NF-kappaB activity and inflammatory response after traumatic brain injury.
Inflammatory response plays an important role in the pathogenesis of acute lung injury (ALI) after traumatic brain injury (TBI). Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key transcription factor that plays a crucial role in cytoprotection against inflammation. The present study explored the influence of Nrf2 genotype on the production of cytokines and on activation of transcription factors in a murine TBI model. ⋯ Nrf2 (-/-) mice were shown to have a greater increase in the lung wet/dry weight ratio compared to their wild-type Nrf2 (+/+) counterparts after TBI. This exacerbation of lung injury in Nrf2 (-/-) mice was associated with increased levels of TNF-alpha, IL-1beta, IL-6, ICAM-1, and their mediator, NF-kappaB. The results suggest that Nrf2 plays an important protective role in attenuating the pulmonary inflammatory response and NF-kappaB activation after TBI.
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Ann. Clin. Lab. Sci. · Jan 2008
Progesterone administration modulates TLRs/NF-kappaB signaling pathway in rat brain after cortical contusion.
This study investigated whether progesterone administration modulates toll-like receptors (TLRs) and the nuclear factor-kappa B (NF-kappaB) signaling pathway in the injured rat brain following traumatic brain injury (TBI). Right parietal cortical contusion was made by a weight-dropping method. Male rats were given 0 or 16 mg/kg injections of progesterone at postinjury hr 1 and 6 and on days 1, 2, 3, 4, and 5. ⋯ Administration of progesterone following TBI down-regulates the cortical levels of these agents related to the TLRs/NF-kappaB signaling pathway. After progesterone administration, apoptotic TUNEL-positive cells in the injured brain were significantly decreased. In summary, post-TBI progesterone administration attenuates the TLRs/NF-kappaB signaling pathway in injured rat brain, and this may be a mechanism whereby progesterone improves the outcome following TBI.