Annals of clinical and laboratory science
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Ann. Clin. Lab. Sci. · Jan 1993
Alterations in von Willebrand factor antigen in premature infants with respiratory distress syndrome and chronic lung disease.
Elevated levels of von Willebrand Factor Antigen (vWF:Ag) may occur in the presence of endothelial injury, a component in the pathology of acute pulmonary insufficiency. The vWF:Ag levels were examined in 13 well infants (controls) and 20 infants with respiratory distress syndrome (RDS), nine of whom developed bronchopulmonary dysplasia (BPD). All infants were very low birth weight (730 to 1500 g) and premature (25 to 34 weeks estimated gestational age). ⋯ Visual examination of vWF multimer patterns revealed absence of unusually large vWF multimers and triplet patterns suggestive of increased proteolytic degradation of von Willebrand factor. However, densitometer scanning revealed that samples with higher vWF:Ag levels (> 200 percent) had increased amounts of moderate to smaller sized multimers, regardless of presence or absence of BPD. It is our conclusion that von Willebrand factor antigen levels are nonspecifically elevated in premature infants and that chronic lung disease is associated with even higher plasma values, possibly owing to pulmonary endothelial injury.
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Ann. Clin. Lab. Sci. · Jan 2009
Recombinant human erythropoietin attenuates spinal neuroimmune activation of neuropathic pain in rats.
Neuropathic pain is a complex syndrome resulting from damage to the peripheral nervous system. Central neuroimmune activation contributes to the generation and maintenance of chronic pain after nerve injury. The current study determined the effects of recombinant human erythropoietin (rhEPO) on behavioral hyperalgesia and neuroimmune activation in a rat model of neuropathic pain induced by L5 spinal nerve transection. ⋯ Furthermore, rhEPO markedly inhibited neuroimmune activation characterized by glial activation, production of proinflammatory cytokines like TNF-alpha, IL-1beta, and NF-kappaB activation, but rhEPO enhanced the level of IL-10. These results support the significance of neuroinflammation and neuroimmune activation in the initiation and persistence of behavioral pain responses. The data indicate that rhEPO attenuates behavioral hyperalgesia and neuroimmune activation in neuropathic pain induced by L5 nerve transection.
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Ann. Clin. Lab. Sci. · Jan 2010
Hydroxyethyl starch 130/0.4 exerts its anti-inflammatory effect in endotoxemic rats by inhibiting the TLR4/NF-kappaB signaling pathway.
Previous studies demonstrated that hydroxyethyl starch (HES) down-regulates the inflammatory response, but the mechanism is controversial. The present study measured the effects of HES130/0.4 on plasma proinflammatory cytokines levels and the Toll-like receptor-4 (TLR4)/nuclear factor-kappa B (NF-kappaB) signaling pathway in lipopolysaccharide (LPS)-treated rats. ⋯ The infusion of HES130/0.4 in endotoxemic rats, especially 15 ml/kg, significantly reduced the release of plasma TNF-alpha and IL-1beta, which was consistent with the observed inhibitory effects of HES130/0.4 on NF-kappaB activation, TLR4 mRNA expression, and TLR4 protein level in monocytes. Thus, HES130/0.4 evidently exerts its anti-inflammatory effect in endotoxemic rats by inhibiting the TLR4/NF-kappaB signaling pathway, which suggests that HES130/0.4 may useful for treating early Gram-negative sepsis.
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Ann. Clin. Lab. Sci. · Nov 1988
Serum copper concentration as an index of cardiopulmonary injury in monocrotaline-treated rats.
The pyrrolizidine alkaloid monocrotaline produces pulmonary inflammation, hemorrhage, fibrosis, and hypertension. In rats, monocrotaline pneumotoxicity can be ameliorated by cotreatment with inhibitors of angiotensin converting enzyme (ACE), such as CL242817. In the present study, serum and urine copper (Cu) concentrations were evaluated as indices of cardiopulmonary injury in rats sacrificed after six weeks of continuous administration of monocrotaline (0 to 3.6 mg per kg per day, in the drinking water) or CL242817 (60 mg per kg per day, in the feed), or both. ⋯ Urinary Cu concentration correlated roughly with that of serum, but the variability within groups was high. Cotreatment with the ACE inhibitor CL242817 not only ameliorated monocrotaline-induced right heart enlargement and lung hydroxyproline accumulation but also reduced the hypercupremia in monocrotaline-treated rats. Thus, serum copper concentration appears to be an accurate and minimally invasive index of monocrotaline pneumotoxicity in this model of pulmonary hypertension.
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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.