A single-site retrospective study of pediatric arterial ischemic stroke etiology, clinical presentation, and radiologic features / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Stroke occurs upon obstruction of cerebral blood circulation and is clinically characterized by sudden onset symptoms. Advanced age is the main risk factor of stroke, but cases of pediatric stroke have been rarely reported. This study aimed to determine the etiology, clinical presentation, and radiologic features of neurological deficit for pediatric arterial ischemic stroke (PAIS).</p><p><b>METHODS</b>The medical records of 42 PAIS patients (age range: 9 months to 13 years) treated at Wuhan Children's Hospital between July 2007 and January 2011 were retrospectively reviewed. Infarction location was first determined by craniocerebral computed tomography and magnetic resonance (MR) imaging. The stenotic or occluded main cerebral arteries and/or branches were determined by MR angiography and digital subtraction angiography.</p><p><b>RESULTS</b>The majority of the 42 PAIS cases (66.7%, n = 28) were ≤ 3 years old (vs. >3 years old: 33.3%, n = 14; P<0.05), but the male: female ratio was similar in both groups (P > 0.05). The most frequently reported signs and symptoms for both age groups were limited physical activity followed by convulsions and delirium, but convulsions were more prevalent in children ≤ 3 years-old. Children > 3 years-old mainly experienced the limited physical activity symptoms, including hemiparalysis, aphasia, and ataxia. For all 42 cases, the most frequent etiologies were infections (38.1%, n = 16), iron deficiency anemia (16.7%, n = 7), and moyamoya syndrome (11.9%, n = 5). The predominant infarcts among all cases were middle cerebral artery (63.6%, n = 21) and basal ganglia (64.3%, n = 27).</p><p><b>CONCLUSIONS</b>PAIS occurs more frequently in younger children and this group most frequently presents with convulsion as the initial symptom. The overall etiologies of PAIS may be different from those of adult stroke and the involved regions may be distinguishing features of PAIS or its different forms, but more research is required.</p>

The role of Src kinase inhibitor ZD6474 on multi-drug resistant K562/A02 cells / 中华血液学杂志

<p><b>OBJECTIVE</b>To investigate the role of Src kinase inhibitor ZD6474 on the growth of multidrug-resistant K562/A02 cells and its regulatory mechanisms.</p><p><b>METHODS</b>The possible mechanisms of drug-resistance were tested by Western blot. Proliferation assays and cell cycle distribution were analyzed by WST metric analysis. Western blot were used to investigate the mechanisms of antiproliferative activity induced by tyrosine kinase inhibitor ZD6474. The in vivo anti-tumor activity was evaluated in K562, K562/A02 xenografted nude mice by administration of ZD6474 (25 - 100 mg×kg(-1)×d(-1), PO).</p><p><b>RESULTS</b>Compared with parental K562 cells, marked high levels of p-Src and Src expression were detected in K562/A02 cells. WST results showed that the IC(50) values of ZD6474 on K562 and K562/A02 after 48 hours incubation were (1.61 ± 0.07) µmol/L and (3.22 ± 0.21)µmol/L, respectively. ZD6474 caused an accumulation of cells in the G(0)/G(1) fraction and apoptosis by inhibiting the expressions of p-Src and Src kinase. Administration of ZD6474 produced a dose-dependent inhibition of tumor growth. 50 mg/kg ZD6474 produced the growth inhibition rates of 43.7% and 56.3%, respectively in K562 and K562/A02.</p><p><b>CONCLUSION</b>Our results indicated that inhibiting Src kinase could induce K562/A02 cells apoptosis in vitro and in vivo.</p>

Repair of finger pulp defect with the homodigital spiral neurovascular island flap / 中国骨伤

<p><b>OBJECTIVE</b>To investigate the method and clinical outcome of reconstructing large pulp defects of the fingertips with a homodigital neurovascular island flap.</p><p><b>METHODS</b>Form June 2007 to October 2009, 16 patients with the defects of pulp were repaired by the spiral flap that was a homodigital neurovascular island flap with a unique spiral advancement and transposition design allowed pulp reconstruction using sensate glabrous skin while restricting donor morbidity to the injured digit. There were 12 males and 4 females with an average age of 37 years ranging from 18 to 49 years. The defect were caused by machine crush injury 11 cases, pressure injury by heavy objects in 2 cases, crush injury by door of car 1 case, injury by saw in 2 cases. The defect was located in the index finger in 5 cases, the middle finger in 9 cases,the ring finger in 2 cases. All injuries had large pulp defects averaging 1.6 cm (long) x 1.2 cm (wide) to 2.5 cm (long) x 1.7 cm (wide). Short-term results for all patients were reviewed. Outcome measures included static 2-point discrimination, total active motion, and hypersensitivity or cold intolerance.</p><p><b>RESULTS</b>All flaps achieved primary healing with no complications. Sensory recovery was excellent with an average 2-point discrimination of 5.1 mm. All patients were followed-up for 8 to 20 months (averaged 12 months) with highly satisfactory with both aesthetic and functional outcome. There was no hypersensitivity or cold intolerance. According to the evaluation of total active motion (TAM) scales, the results were excellent in 7 cases, good in 8 cases (9 lesions) and fair in 1 case.</p><p><b>CONCLUSION</b>The spiral advancement-transposition flap is suitable for resurfacing large pulp defects with excellent short-term functional and aesthetic results and high patient satisfaction.</p>

Effect of ZD6474 on the proliferation of imatinib-resistant K562 cells / 中华血液学杂志

<p><b>OBJECTIVE</b>To investigate the effect of tyrosine kinase inhibitor ZD6474 (Vandetanib) on the proliferative inhibition of K562 cells and its derived imatinib-resistant K562/G cells and its mechanism.</p><p><b>METHODS</b>Imatinib-resistant K562/G cells were obtained by culturing cells in gradually increasing concentrations of imatinib. The changed factors related to drug-resistance were tested by Western blot. ZD6474 and imatinib affected K562/G and parental K562 cells proliferation were analyzed by WST assay. Flow cytometry was used to analyze cell cycle. Direct inhibition of Src activity by ZD6474 was measured by a colorimetric ELISA assay with recombinant human Src kinase.</p><p><b>RESULTS</b>10 µmol/L imatinib failed to inhibit K562/G cells proliferation or induce cell cycle arrest. Compared with that in parental K562 cells, there were marked high levels of p-Src and Src protein in K562/G cells. The expression of Bcl-2 and p-STAT3 also increased in K562/G cells. After 48 hours incubation, the IC(50) values of ZD6474 in K562 and K562/G cells were 1.61 µmol/L and 3.18 µmol/L, respectively. ZD6474 treatment caused accumulation of cells in the G(0)/G(1) fraction and cell apoptosis in K562 and K562/G cells. ZD6474 decreased the expression of p-Src and Src at post-transcriptional level. Moreover, ZD6474 increased the ratio of Bax/Bcl-2 and decreased the expression of p-STAT3 at the same concentration for inducing apoptosis.</p><p><b>CONCLUSIONS</b>ZD6474 is effective in inhibiting the proliferation of imatinib-resistant K562/G cells and parental K562 cells, and induces their apoptasis by significant inhibition of Src kinase activity. Our study provides a reliable experimental basis for chronic myeloid leukemia treatment with ZD6474.</p>

Significance of Biological Rhythm on Selective Nocte Treatment on Autosomal Dominant Nocturnal Frontal Lobe Epilepsy / 实用儿科临床杂志

0.05).The adverse effect of treatment group was significantly less than control group(P