Biological Effects of Chitosan-Based Dressing on Hemostasis Mechanism.

There have been numerous recent advances in wound care management. Nevertheless, the assessment of hemostatic dressing is essential to enable surgeons and other physicians and healthcare professionals to make the correct decisions regarding the disposition of severe hemorrhage. Here, we investigated the relative efficacies of chitosan-based and conventional gauze dressings in a rat model of femoral artery hemorrhage and in patients with surgical wounds. Dressing effectiveness was evaluated based on hemostatic profiles, biocompatibility, antimicrobial activity, and blood factor responses in coagulation. Relative to standard gauze dressing, the chitosan fiber (CF) dressing treatment significantly shortened the time to hemostasis in injured rats. Moreover, the CF dressing significantly prolonged partial thromboplastin time, enhanced blood absorption, and reduced antithrombin production without altering the prothrombin ratio. Unlike regular gauze bandages, the CF dressing demonstrated remarkable antibacterial activity. The results of this study indicate the effectiveness of chitosan as a hemostatic dressing and elucidate its underlying mechanism. It is possible that chitosan surgical dressings could serve as first-line intervention in hospital emergency care for uncontrolled hemorrhage.

Infantile form of muscle phosphofructokinase deficiency in a premature neonate.

Muscle phosphofructokinase (PFK) deficiency is a rare autosomal recessive disease. We report the case of a preterm female infant who was diagnosed with the infantile form of phosphofructokinase deficiency due to a lack of PFK activity in her muscles, manifesting at a corrected age of 1 month as floppy infant syndrome, congenital joint contracture, cleft palate and duplication of the pelvicalyceal system. She died at a corrected age of 6 months due to respiratory failure. We further reviewed other infantile cases in the literature. Congenital hypotonia (78.6%), arthrogryposis (64.3%) and other systemic involvement including encephalopathy (35.7%) and cardiomyopathy (21.4%) are common presentations of the infantile form of PFK deficiency. The overall survival rate of the infantile form is low. The early recognition of multiple system involvement is essential to provide better clinical care for infants with the infantile form of PFK deficiency.

Neurogenesis recovery induced by granulocyte-colony stimulating factor in neonatal rat brain after perinatal hypoxia.

BACKGROUND: Perinatal hypoxia can lead to a wide range of neurological deficits depending on the differential vulnerability of the involved brain regions to oxygen deprivation. It remains unclear whether the differential vulnerability to oxygen deprivation leads to altered neurogenesis in the neonatal brain after perinatal hypoxia. The primary objective was to investigate whether perinatal hypoxia induces deleterious changes in neurogenesis within three representative brain regions (dentate gyrus of the hippocampus, midbrain, and temporal cortex), with regards to common pathological areas clinically. The secondary objective was to investigate whether granulocyte-colony stimulating factor (G-CSF) therapy exerts beneficial effects in neurogenesis in neonatal rat brains subjected to experimental perinatal hypoxia. MATERIALS AND METHODS: Rat pups were subjected to experimental perinatal hypoxia on the tenth day of life (P10). They were then given G-CSF (30 µg/kg, single injection/day, intraperitoneal injection, P11-16). The neurogenesis efficacy was analyzed on P17 and the radial-arm maze task, a memory task for higher cognitive functions such as problem-solving abilities, was evaluated on P37-58. RESULTS: Perinatal hypoxia caused a significant decrease in neurogenesis within the three representative brain regions, and this deleterious outcome was alleviated by G-CSF (p < 0.05). In addition, the G-CSF therapy markedly improved the decreased performance of long-term cognitive functions induced by perinatal hypoxia (p < 0.05). CONCLUSION: This study suggests that G-CSF may be a potentially beneficial therapy, at least in part, through universal recovery of neurogenesis effects in the neonatal brain after perinatal hypoxia insult.

The clinical implications of ABO blood groups in Pseudomonas aeruginosa sepsis in children.

BACKGROUND: Pseudomonas aeruginosa (P. aeruginosa) sepsis is a fetal disease with rapid progressive shock for infants and children in hospital and in the community, without initial treatment with appropriate antibiotics. Because underlying risk factors remain unclear for affected patients, it is still difficult for early diagnosis and therapy. Recently, ABO blood group antigens were associated with several infectious diseases. However, it was not reported whether the ABO blood group could be the clinical implications for pediatric Pseudomonas sepsis. METHODS: This study retrospectively reviewed the medical records of 23 infants and children with P. aeruginosa sepsis, who were hospitalized at Kaohsiung Chang Gung Memorial Hospital from 2003 to 2009. RESULTS: Eight cases had nosocomial infections, with a higher mortality rate (50%) than 15 cases (26.7%) in the community. Thirteen patients (86.7%) with community-acquired sepsis were infants, significantly younger than the nosocomial cases. ABO blood group antigens were known in 21 cases and B phenotype was the most significant. In the community-acquired group, fever and diarrhea were the most prevalent symptoms on initial presentation. Moreover, pneumonitis was the most concomitant disease in fatal cases. CONCLUSION: Blood group B was highly associated with pediatric P. aeruginosa sepsis. This could be a risk factor, and play an important role for the pathogenesis of P. aeruginosa sepsis. Furthermore, if a previously healthy infant with fever and diarrhea suddenly had septic presentation, P. aeruginosa infection should be considered. In addition, more intensive care could be needed for such blood group B pediatric patients, if pneumonitis was concomitant on admission for the high mortality rate.

Granulocyte-colony stimulating factor alleviates perinatal hypoxia-induced decreases in hippocampal synaptic efficacy and neurogenesis in the neonatal rat brain.

Using various animal models, studies have greatly expanded our understanding of perinatal hypoxia-induced neuronal injury in the newborn at the cellular/molecular levels. However, the synapse-basis pathogenesis and therapeutic strategy for such detrimental alterations in the neonatal brain remain to be addressed. We investigated whether the damaged synaptic efficacy and neurogenesis within hippocampal CA1 region (an essential integration area for mammalian learning and memory) of the neonatal rat brain after perinatal hypoxia were restored by granulocyte-colony stimulating factor (G-CSF) therapy. Ten-day-old (P10) rat pups were subjected to experimentally perinatal hypoxia. G-CSF (10, 30, or 50 µg/kg, single injection/d, P11-16) was s.c. administered to neonatal rats which were analyzed on P17. Perinatal hypoxia reduced the expression in pRaf-pERK1/2-pCREB(Ser-133) signaling, the synaptic complex of postsynaptic density protein-95 (PSD-95) with N-methyl-D-aspartate receptor (NMDAR) subunits (NR1, NR2A, and NR2B), synaptic efficacy, and neurogenesis. A representatively effective dosage of G-CSF (30 µg/kg) alleviated the perinatal hypoxia-induced detrimental changes and improved the performance in long-term cognitive function. In summary, our results suggest a novel concept that synaptic efficacy defects exist in the neonatal brain previously exposed to perinatal hypoxia and that G-CSF could be a clinical potential for the synapse-basis recovery in the perinatal hypoxia suffers.