Annals of clinical and laboratory science
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Ann. Clin. Lab. Sci. · Jan 2012
A combination of CD15/CD10, CD64/CD33, CD16/CD13 or CD11b flow cytometric granulocyte panels is sensitive and specific for diagnosis of myelodysplastic syndrome.
Flow cytometry (FCM) is a reproducible and objective technique that may be useful in the diagnosis of myelodysplastic syndrome (MDS) by detecting abnormal immunophenotypes specific to MDS. We investigated 5 granulocyte/monocyte panels by FCM to find a sensitive and specific combination of panels in order to discriminate MDS from non-clonal hematologic disorders. Bone marrow aspirates from 35 patients with MDS and 25 patients with non-clonal hematologic disorders were studied. ⋯ As the number of employed panels increased, the percent values of abnormal immunophenotypes increased (P=0.002). The maximum rate of abnormal immunophenotype was 89.7% in MDS patients, especially 100.0% in normal karyotype, when a combination of three panels, CD15/CD10/CD45, CD64/CD33/CD45, and either CD16/CD13/CD45 or CD16/CD11b/CD45 was used. This study demonstrates that a combination of CD15/CD10, CD64/CD33, CD16/CD13 or CD11b granulocyte panels in FCM is sensitive and specific for diagnosis of MDS.
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Ann. Clin. Lab. Sci. · Jan 2012
Case ReportsSLC22A5 mutations in a patient with systemic primary carnitine deficiency: the first Korean case confirmed by biochemical and molecular investigation.
Systemic primary carnitine deficiency (CDSP) is a rare autosomal recessive disorder that presents episodic periods of hypoketotic hypoglycemia. The main symptoms of CDSP are skeletal and cardiac myopathy. CDSP is caused by a defect in plasma membrane uptake of carnitine, ultimately caused by the SLC22A5 gene. ⋯ The patient was treated with L-carnitine to reach a normal free carnitine level and has remained asymptomatic up to the current age of 21 months. The plasma free carnitine level normalized to 66.6 μmol/L at 4 weeks after treatment. To the best of our knowledge, this is the first report of a CDSP patient confirmed by molecular genetic investigation.
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Ann. Clin. Lab. Sci. · Jan 2012
Procalcitonin levels within 48 hours after burn injury as a prognostic factor.
This study was performed to evaluate the clinical significance of procalcitonin in burn patients and to investigate whether procalcitonin levels at admission can be a prognostic indicator for sepsis and mortality. ⋯ Procalcitonin concentrations determined within the first 48 hours after burn injury can be a useful prognostic indicator for sepsis and mortality in burn patients.
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Ann. Clin. Lab. Sci. · Jan 2012
Chronic paracetamol treatment influences indices of reactive oxygen species accumulation in the aging Fischer 344 X Brown Norway rat aorta.
Previous reports have demonstrated that increased levels of reactive oxygen species (ROS) and alterations in cell signaling characterize aging in the Fischer 344 X Brown Norway (FBN) rat aorta. Other work has suggested that increases in ROS may be related to vascular wall thickening and the development of hypertension. Paracetamol (acetaminophen) is a potent antioxidant that has been found to diminish free radicals in ischemia-reperfusion studies. ⋯ Chronic paracetamol treatment decreased tunica media thickness and the amount of oxidized protein by 13 ± 4% and 30 ± 1%, respectively (p ≤0.05). This finding of diminished aortic thickening was associated with increased phosphorylation (activation) of the mitogen activated protein kinases and diminished levels of the anti-apoptotic protein Bcl-2. Taken together, these data suggest that chronic paracetamol treatment may decrease the deleterious effects of aging in the FBN rat aorta.
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Ann. Clin. Lab. Sci. · Jan 2012
Genetic ablation of toll-like receptor 2 reduces secondary brain injury caused by cortical contusion in mice.
Previous studies have shown that Toll-like receptor 2 (TLR2) was up-regulated after traumatic brain injury (TBI), but the potential contribution of TLR2 to TBI still remains unclear. The present study investigated the role of TLR2 in modulating TBI-induced secondary brain injury in mice. Wild-type TLR2(+/+) and TLR2(-/-)-deficient mice were subjected to a moderately severe weight-drop impact head injury. ⋯ We measured TLR2 by western blot; motor function by Grip test; brain edema by wet/dry method; cortical apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method; and IL-1β, TNF-α and IL-6 by enzyme-linked immunosorbent assay (ELISA). We found the absence of TLR2 function in mice resulted in amelio-rating brain injury as shown by the reduced severity of neurological deficit, apoptosis, and brain edema at 24 hours after TBI, which was associated with the decreased expression of inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), compared with their wild-type counterparts after TBI. In combination, these results suggest that TLR2 might play an important aggravating role in the pathogenesis of TBI-induced secondary brain injury, possibly by regulating inflammatory cytokines in the cortex.