贫困县小学生睡眠状况调查

目的:了解贫困地区小学生睡眠状况,探讨提高农村儿童睡眠质量的有效措施。方法:于2005-10在吉林省的国家级贫困县应用澳大利亚悉尼大学儿童睡眠中心临床问卷的中国修订版(内容涉及儿童个人情况、睡眠状况、家庭居住环境,父母睡眠状况、吸烟状况,以及父母职业及受教育程度、家庭成员之间的关系等),采用二阶段整群随机抽样法,对750名小学生的睡眠状况进行调查分析,统计分析近1年内儿童在未患重大疾病时的睡眠状况,包括全天睡眠时间分布状况、睡眠障碍发病率及其相关影响因素,根据美国精神障碍诊断统计手册中儿童睡眠障碍的诊断标准,将每周出现1～3次单一或几种睡眠障碍相关症状,定为存在睡眠问题。结果:共发放问卷750份,回收有效问卷691份,回收率为92.1%。6岁和13岁组人数较少予以去除,实际纳入分析者669名。其中男生300名,女生369名;汉族361名,朝鲜族288名,其他民族20名;7岁组96名,8岁组93名,9岁组94名,10岁组122名,11岁组128名,12岁组136名。①贫困县小学生全天睡眠时间均值为(9.62±1.12)h,汉族小学生全天平均睡眠时间比朝鲜族学生长[(9.75±1.23),(9.48±0.90)h,P<0.01]。各年龄组学生全天睡眠时间差异无统计学意义(F=0.169,P>0.05)。②睡眠障碍总时点发病率为27.40%。低年级组小学生(一～四年级)睡眠障碍发病率高于高年级组(五～六年级)(31.80%,24.15%,P<0.05),男生睡眠障碍发病率高于女生(35.35%,20.95%,P<0.01)。③睡眠障碍症状发病率前5位依次为:睡眠不安(8.4%),睡眠姿势异常(8.3%)、张口呼吸(6.1%),梦呓(5.2%);打鼾(4.3%)。④调查结果经单因素相关分析及多重逐步回归分析显示抚养人睡眠习惯、儿童睡眠姿势异常、母亲管教孩子态度和父亲学历等是影响睡眠时间的主要因素。⑤Logistic回归分析显示,孩子患呼吸系统疾病、父母教育孩子方法、母亲有无睡眠障碍、父母之间关系、儿童体弱多病等是睡眠障碍的主要危险因素。结论:贫困地区儿童睡眠障碍是多因素共同作用的结果;孩子的抚养人应改掉不良的睡眠习惯,为儿童提供良好的生活、睡眠环境;增强儿童身体素质,积极防治呼吸系统疾病,应作为近期降低贫困县小学生睡眠障碍的有效措施。     

Fatal necrotizing pneumonia caused by Panton-Valentine leukocidin-producing hospital-acquired Staphylococcus aureus: a case report

Panton-Valentine leukocidin (PVL) is a cytotoxin which causes leukocyte destruction and tissue necrosis. Although it is produced by fewer than 5% of Staphylococcus aureus strains, PVL-producing S. aureus is emerging as a serious problem worldwide. There has been a marked increase in the incidence of necrotizing lung infections with a very high mortality associated with these strains. This report describes a fatal case of hospital-acquired necrotizing pneumonia caused by PVL-positive methicillin-susceptible S. aureus in a patient with a brain tumor.     

Colorectal Cancer Liver Metastasis Trends in the Kingdom of Saudi Arabia

Background/Aim:To elucidate colorectal cancer (CRC) disease patterns, demographics, characteristics, stage at presentation, metastases, and survival rates of patients, particularly those with liver metastases, at our center as the first report from the Kingdom of Saudi Arabia.Results:427 cases of CRC with a mean age at diagnosis of 55.47 ± 12.85 years, out of which 96% were resected. Stage II was predominant at presentation, followed by both stage III and IV, with the remainder being stage I. One hundred patients had distant metastases, of which the liver was the only location in 54 patients. Mean survival was 3.0 years. Overall survival rates for CRC patients with liver metastases who underwent resection were 30% at 2 years and 17% at 5 years, and the mean survival rate was 1.4 years.Conclusions:Both the mean survival rate of our CRC patients with resectable liver metastases and the 5-year survival rate of these patients are lower than global averages. This discrepancy is likely due to late diagnoses rather than more aggressive disease.Key Words: Colon cancer, metastasis, Saudi Arabia, survivalColorectal cancer (CRC) is considered to be the third most common malignancy worldwide.[1] It affects roughly 30–50 people per 100,000 individuals in the USA and Europe,[2] and roughly half of these patients develop metastases during the course of the disease.[3,4] The liver is the predominant site of metastasis in CRC, and 25% of patients present with metastases at the time of diagnosis (synchronous).[4,5,6] Throughout the course of the disease, in particular after resection of the primary tumor, approximately half of all CRC patients develop liver metastases.[4,5,6] CRC rates are markedly lower in Africa and the Middle East, occurring at an estimated rate of 3–11 per 100,000 individuals.[7] Specifically, in the Kingdom of Saudi Arabia (KSA), the incidence of CRC is increasing from 6.6 per 100,000 individuals in 2003[8] to over 12 per 100,000 individuals in 2008.[9]In a recent meta-analysis by Kanakas et al., the global 3 and 5-year mean survival rates of CRC were estimated to be 57.6 and 40.3%, respectively;[10] however, 5-year survival rates in the USA are estimated to be greater than 65%.[11] In comparison, the 5-year survival rate of CRC in the KSA is reported to be 44.6%.[12] Survival rates have improved tremendously for CRC due to early detection, application of total mesorectal excision, and addition of radiochemotherapy.[13,14] With respect to CRC patients with liver metastases, the estimated global mean 5-year survival is 38%, although this number varies dramatically from region to region.[10] Survival improvement for metastatic CRC is majorly due to the aggressive surgical approach in resecting all metastasis and the addition of effective systemic chemotherapy.[15] Despite increasing data pertaining to CRC incidence and survival in the KSA, information relating to the leading cause of death from this disease, namely liver metastasis, is currently scarce.[16] Therefore, the aim of this study is to elucidate CRC disease pattern and survival rates, particularly of patients with liver metastases, in the KSA population and to compare these figures to the global averages.     

女子体操运动员控制体质量与营养调控的效果：个案分析

目的:寻求适合女子体操运动员的控制体质量和营养补充的科学方法。方法:以1名女子体操运动员为观察对象,年龄17岁,训练年限14年,体质量51.6kg,身高150cm。身体健康,且对干预方案和监测指标知情同意。运动员减重前的体成分:体质量51.6kg,肌肉重量37.1kg,脂肪11.8kg,体脂百分比22.9%,总水含量29.1kg,该运动员的体脂较高,减重的主要部分为脂肪。采用缓慢减重、饮食控制和增加运动量相结合的方法减轻和控制体质量。进行为期12周的体质量干预,每周减重1kg,稳定1周。在制定减重期间的食谱时,把运动员全日的总能量控制在2000～2500kJ,食谱中将脂肪的百分比控制在20%以下,蛋白质增至35%～40%,碳水化合物的比例相对控制在40%～45%。在减重期间增加有氧运动以减少脂肪含量。1d的有氧训练方案:慢跑(约200m/min,50%～60%最大吸氧量)30min,以6.0km/h,4%的坡度在跑步机上跑40min,小重量多次数多组数的力量练习,尤其是腰腹部位的练习。有氧运动每周进行6次。基本保持运动员每天训练和有氧运动消耗的热量为4.2～6.3MJ。结果:①体质量和体脂变化:运动员在减控体质量方案实施12周内,体质量减少了5.4kg,其中脂肪为5.0kg,肌肉减少0.2kg,体脂百分比从22.9%减至14.8%。②运动员功能状态:在减重的初期,运动员自我感觉到疲劳、饥饿,但尚能忍受,每天能坚持训练。此不适持续3～5d后症状逐渐减轻,1周后运动员精神状态恢复,自觉体能状态好,技术动作完成准确。在减重期间定期给运动员检查血常规,减重前血常规值为134g/L,减重的第3周起血常规值上升至146g/L,此后保持在146～149g/L,提示在减重期间运动员的身体机能状况有所提高。结论:体操运动员减轻和控制体质量应用饮食控制和增加运动量相结合的方法,以缓慢的能量负平衡为主,同时监测身体功能状况;减重过程中要科学地安排膳食和补充营养。     

Bone matrix degradation by the plasminogen activation system. Possible mechanism of bone destruction in arthritis

The observed increase in urokinase-type plasminogen activator (u-PA) and its receptor (u-PAR) in synovial tissue of patients with rheumatoid arthritis (RA) suggests pathophysiological involvement of the plasminogen activation (PA) system in inflammatory joint disease. In the present study, we investigated the capacity of the PA system to degrade non-mineralized and mineralized bone-like matrix in vitro as a model for bone destruction. Transfected mouse LB6 cell lines, that expressed either human u-PA or u-PAR, were cultured separately and simultaneously on radiolabelled bone matrix in the presence of plasminogen. Osteoblast-like murine calvarial MC3T3-E1 cells were used to produce a well-characterized, highly organized bone-like matrix, that could be mineralized in the presence of beta-glycerol phosphate. Bone matrix degradation was followed by the release of radioactivity in the culture medium. u-PA-producing cells, in contrast to u-PAR- producing cells, degraded both non-mineralized and mineralized bone matrix. This effect could be inhibited by anti-u-PA antibodies, as well as by tranexamic acid and by aprotinin, indicating that the degrading activity is u-PA mediated and plasmin dependent. Co-cultivation of a small portion of u-PA-producing cells with u-PAR-expressing cells resulted in a marked increase in degradation activity. Reduction of this potentiating effect by suramin or the amino-terminal fragment of u- PA, both competitive inhibitors of u-PA receptor binding, shows that this synergistic effect is due to binding of u-PA to u-PAR. u-PAR must be cell associated, as binding of u-PA to a soluble u-PAR prevented this enhancement. The capability of the PA system to degrade bone matrix in vitro, and the previously demonstrated increased expression of u-PA and u-PAR in synovial tissue of patients with RA, further support a role for the PA system in the development of bone erosions.      

Radiographic damage in large joints in early rheumatoid arthritis: relationship with radiographic damage in hands and feet, disease activity, and physical disability

An assessment of the onset of radiographic damage in the large joints (hip, knees, shoulders, elbows, ankles and tarsus) in patients with early rheumatoid arthritis, and the relationship of the progression of large joint damage with joint damage in hands and feet, with physical disability, and with cumulative disease activity, was performed in a prospective 6 yr follow-up study. Large joint damage appeared to be an early phenomenon with 20% of the patients having some damage in at least one large joint within 1 yr, and 50% of the patients within 6 yr after disease onset. Radiographic damage in large joints was significantly related to the damage in hands and feet, the physical disability index, and the cumulative disease activity. The initial disease activity at study entry was the only prognostic factor that reached significance.      

An essential role for lysophosphatidylcholine in the inhibition of platelet aggregation by secretory phospholipase A2

The release of secretory phospholipase A2 (sPLA2) into the mammalian circulation may contribute to the development of hemorrhagic and inflammatory diseases. sPLA2 has previously been shown to alter the behavior of platelets, leukocytes, and endothelial cells, although the molecular basis for these cellular effects has not been established. Our studies indicate that the inhibition of platelet aggregation by snake, bee venom, and pancreatic sPLA2 is dependent on a plasma cofactor. This cofactor resides within the lipoprotein fraction of plasma, with 54%, 31%, and 11% of the activity present in the high- density lipoprotein (HDL), low-density lipoprotein (LDL), and very low density lipoprotein (VLDL) fractions, respectively. Delipidation of HDL and LDL was associated with the complete loss of platelet-inhibitory activity. Incubation of purified sPLA2 with the HDL fraction of plasma resulted in the time-dependent generation of lysophosphatidylcholine (lysoPC). The formation of lysoPC correlated with the inhibition of platelet aggregation. Purified lysoPC (10 to 100 micrograms/mL) inhibited platelet aggregation and dense granule release induced by thrombin (0.05 U/mL), collagen (1 micrograms/mL), ionophore A23187 (2 mumol/L), ADP (12.5 mumol/L), and adrenaline (3.2 mumol/L). The inhibition of platelet aggregation by lysoPC was dose-dependent and correlated with decreased fibrinogen binding to glycoprotein IIb-IIIa. Our studies indicate that the enzymatic generation of lysoPC from plasma lipoproteins is essential for the sPLA2-mediated inhibition of platelet activation in the presence of albumin. These results raise the possibility that the toxic effects of circulating sPLA2 may be due in part to the generation of the bioactive lysophospholipid, lysoPC.     

Factor VIII gene inversions in severe hemophilia A: results of an international consortium study

Twenty-two molecular diagnostic laboratories from 14 countries participated in a consortium study to estimate the impact of Factor VIII gene inversions in severe hemophilia A. A total of 2,093 patients with severe hemophilia A were studied; of those, 740 (35%) had a type 1 (distal) factor VIII inversion, and 140 (7%) showed a type 2 (proximal) inversion. In 25 cases, the molecular analysis showed additional abnormal or polymorphic patterns. Ninety-eight percent of 532 mothers of patients with inversions were carriers of the abnormal factor VIII gene; when only mothers of nonfamilial cases were studied, 9 de novo inversions in maternal germ cells were observed among 225 cases (approximately 1 de novo maternal origin of the inversion in 25 mothers of sporadic cases). When the maternal grandparental origin was examined, the inversions occurred de novo in male germ cells in 69 cases and female germ cells in 1 case. The presence of factor VIII inversions is not a major predisposing factor for the development of factor VIII inhibitors; however, slightly more patients with severe hemophilia A and factor VIII inversions develop inhibitors (130 of 642 [20%]) than patients with severe hemophilia A without inversions (131 of 821 [16%]).     

A comparative study of the iron-clearing properties of desferrithiocin analogues with desferrioxamine B in a Cebus monkey model

A comparative study of the iron-clearing properties of subcutaneously administered desferrioxamine B (DFO) with those of orally administered desferrithiocin sodium salt (1), desmethyl desferrithiocin (2), desazadesmethyl desferrithiocin sodium salt (3), desazadesmethyl desferrithiocin pivaloyloxymethyl ester (4), and desazadesmethyl-5,5- dimethyl desferrithiocin (5) in an iron-loaded Cebus monkey model and a non-iron overloaded bile duct-cannulated rat model is presented. All six drugs, which performed well in rodent studies, demonstrated increased efficiency in the Cebus monkey model. When administered to rodents at a daily dosage of 384 mumol/kg over a period of 10 days, drug 1 demonstrated severe renal toxicity. whereas drugs 3, 4, and 5 exhibited severe gastrointestinal (GI) toxicity. Under the same experimental protocol, drug 2 did not show significant toxic side effects. In addition, to further evaluate the iron-clearing properties of analogue 2, a dose-response study was performed in the primates that showed that iron excretion increased in a dose-dependent fashion.