儿童阻塞性睡眠呼吸暂停低通气综合征上气道结构的MRI研究分析

目的利用磁共振成像（MRI）对儿童阻塞性睡眠呼吸暂停低通气综合征（OSAHS）的上气道结构进行测量分析,探讨儿童OSAHS上气道的结构特点。方法选择原发性鼾症组（Ps组）30例和OSAHS组30例,同时随机选择30例正常儿童作为对照组,应用MRI对上气道进行空间测量和软组织测量,结果进行统计学分析。结果①空间测量：3组儿童之间相比,鼻咽气道截面积、口咽气道截面积、腭咽气道截面积、气道斜径,比较差异有统计学意义（P〈0．05）;②软组织测量：舌体截面积3组之间差异无统计学意义（P〉0．05）;OSAHS组比Ps组及对照组腺样体截面积大、腺样体斜距长,比较有统计学意义（P〈0．05）;OSAHS组、Ps组比对照组扁桃体截面积大,比较有统计学意义（P〈0．05）。结论应用MRI可以判定OSAHS儿童上气道的狭窄情况,可作为诊断儿童OSAHS的重要辅助手段。     

Incidence and factors associated with cardiac arrest complicating emergency airway management

Objective

Cardiac arrest (CA) is a rare but recognized complication of emergency airway management. Our aim was to measure the incidence of peri-intubation CA during emergency intubation and identify factors associated with this complication.

Methods

Retrospective cohort study of emergency endotracheal intubations performed in a large, urban emergency department over a one-year period. Patients were included if they were >18 years old and not in CA prior to intubation. Multiple logistic regression modeling was used to define factors independently associated with CA.

Results

A total 542 patients underwent emergency intubation during the study period and 410 met inclusion criteria for this study. CA occurred in 17/410 (4.2%) at a median of 6 min post-intubation. Nearly two-thirds of CA events occurred within 10 min of drug induction; early peri-intubation CA rate 2.4% (95% CI: 1.3–4.5%). Pulseless electrical activity was the initial rhythm in the majority of cases. More than half of CA events were successfully resuscitated but CA was associated with increased odds of hospital death (OR 14.8; 95% CI: 4.2–52). Pre-intubation hemodynamic and oximetry variables were associated with CA. CA was more common in patients experiencing pre intubation hypotension (12% vs 3%; p < 0.002). Pre RSI shock index (SI) and weight were independently associated with CA.

Conclusions

In this series, 1 in 25 emergency intubations was associated with the complication of CA. Peri-intubation CA is associated with increased mortality. Pre-intubation patient characteristics are associated with this complication.     

Diminished ICAM-1 expression and impaired pulmonary clearance of nontypeable Haemophilus influenzae in a mouse model of chronic obstructive pulmonary disease/emphysema

The airways of patients with chronic obstructive pulmonary disease (COPD) are continually colonized with bacterial opportunists like nontypeable Haemophilus influenzae (NTHi), and a wealth of evidence indicates that changes in bacterial populations within the lung can influence the severity of COPD. In this study, we used a murine model for COPD/emphysema to test the hypothesis that COPD affects pulmonary clearance. Mice were treated with a pulmonary bolus of elastase, and as reported previously, the lungs of these mice were pathologically similar to those with COPD/emphysema at ~1 month posttreatment. Pulmonary clearance of NTHi was significantly impaired in elastase-treated versus mock-treated mice. While histopathologic analysis revealed minimal differences in localized lung inflammation between the two groups, lower levels of intercellular adhesion molecule 1 (ICAM-1) were observed for the airway epithelial surface of elastase-treated mice than for those of control mice. Following infection, elastase-treated mice had lung pathology consistent with pneumonia for as long as 72 h postinfection, whereas at the same time point, mock-treated mice had cleared NTHi and showed little apparent pathology. Large aggregates of bacteria were observed within damaged lung tissue of the elastase-treated mice, whereas sparse individual bacteria were observed in lungs of mock-treated mice at the same time point postinfection. Additional infection studies showed that NTHi mutants with biofilm defects were less persistent in the elastase-treated mice than the parent strain. These findings establish a model for COPD-related infections and support the hypotheses that ICAM-1 promotes clearance of NTHi. Furthermore, the data indicate that NTHi may form biofilms within the context of COPD-related infections.     

硼替佐米联合地塞米松与沙利度胺治疗多发性骨髓瘤的效果

目的比较硼替佐米＋地塞米松＋沙利度胺（BDT）方案与长春地辛＋表柔比星＋地塞米松＋沙利度胺（VADT）方案治疗多发性骨髓瘤（MM）的临床效果。方法MM病人67例,应用BDT方案治疗30例,VADT方案治疗37例,均治疗4个疗程,比较两组治疗前、治疗后β2-微球蛋白、免疫球蛋白、骨髓瘤细胞的变化,并比较两组疗效。结果BDT组及VADT组化疗后β2-微球蛋白、免疫球蛋白、骨髓瘤细胞均低于化疗前,差异有显著性（t=2．837～7．562,P％0．05）。BDT组完全缓解（CR）占13．0％,接近完全缓解（ncR）占20．0％,部分缓解（PR）占53．0％,微小反应（MR）占6．7％,总有效率93．3％;VADT组CR占3．0％,nCR占10．8％,PR占40．5％,MR占16．2％,总有效率70．3％,两组疗效比较,差异有显著性（Hc=51．67,P〈0．05）。结论BDT方案治疗MM效果优于VADT方案,且起效快,可改善病人的预后。     

Interferon-γ: Promising therapeutic target in atherosclerosis

Atherosclerosis is a chronic inflammatory disorder of the vasculature and is the primary cause of cardiovascular disease(CVD). CVD is currently the world's leading cause of death and the numbers are predicted to rise further because of a global increase in risk factors such as diabetes and obesity. Current therapies such as statins have had a major impact in reducing mortality from CVD. However, there is a marked residual CVD risk in patients on statin therapy. It is therefore important to understand the molecular basis of this disease in detail and to develop alternative novel therapeutics. Interferon-γ(IFN-γ) is a pro-inflammatory cytokine that is often regarded as a master regulator of atherosclerosis development. IFN-γ is able to influence several key steps during atherosclerosis development, including pro-inflammatory gene expression, the recruitment of monocytes from the blood to the activated arterial endothelium and plaque stability. This central role of IFN-γ makes it a promising therapeutic target. The purpose of this editorial is to describe the key role IFN-γ plays during atherosclerosis development, as well as discuss potential strategies to target it therapeutically.     

p53‐Based strategy to reduce hematological toxicity of?chemotherapy: A proof of principle study

p53 activation is a primary mechanism underlying pathological responses to DNA damaging agents such as chemotherapy and radiotherapy. Our recent animal studies showed that low dose arsenic (LDA)‐induced transient p53 inhibition selectively protected normal tissues from chemotherapy‐induced toxicity.Study objectives were to: 1) define the lowest safe dose of arsenic trioxide that transiently blocks p53 activation in patients and 2) assess the potential of LDA to decrease hematological toxicity from chemotherapy.Patients scheduled to receive minimum 4 cycles of myelosuppressive chemotherapy were eligible. For objective 1, dose escalation of LDA started at 0.005 mg/kg/day for 3 days. This dose satisfied objective 1 and was administered before chemotherapy cycles 2, 4, and 6 for objective 2. p53 level in peripheral lymphocytes was measured on day 1 of each cycle by ELISA assay. Chemotherapy cycles 1, 3, and 5 served as the baseline for the subsequent cycles of 2, 4, and 6 respectively. If p53 level for the subsequent cycle was lower (or higher) than the baseline cycle, p53 was defined as “suppressed” (or “activated”) for the pair of cycles. Repeated measures linear models of CBC in terms of day, cycle, p53 activity and interaction terms were used.Twenty‐six patients treated with 3 week cycle regimens form the base of analyses. The mean white blood cell, hemoglobin and absolute neutrophil counts were significantly higher in the “suppressed” relative to the “activated” group.These data support the proof of principle that suppression of p53 could lead to protection of bone marrow in patients receiving chemotherapy.This trial is registered in ClinicalTrials.gov. Identifier: {"type":"clinical-trial","attrs":{"text":"NCT01428128","term_id":"NCT01428128"}}NCT01428128.     

称重法和化学分析法评估人群膳食矿物质摄入量的比较

目的 探讨称重法和化学分析法评估人群矿物质摄入量的差异和相关性.方法 同时使用称重法和化学分析法对89名上海市居民进行膳食调查,并对两种调查方法测得的钙、镁、铁、锌、铜、锰摄入量进行比较分析.结果 称重法调查的6种矿物质元素的摄入量高于化学分析法(P<0.05),称重法调查的平均每天钙、镁、铁、锌、铜、锰摄入量比化学分析法分别高20.9%、67.4%、19.5%、84.4%、46.7%和33.3%;称重法与化学分析法测得的钙、镁、铁、锌、铜、锰摄入量均呈显著正相关(P<0.01),相关系数分别为0.571、0.672、0.521、0.524、0.538和0.691.结论 称重法测得的人群膳食矿物质摄入量高于化学分析法.     

Factors causing malnutrition in patients with chronic uremia

There is abundant evidence that patients with chronic renal failure (CRF), including those treated by hemodialysis or peritoneal dialysis, have evidence of malnutrition with decreased body weight and subnormal values of serum proteins (suggesting a loss of visceral protein stores). Potential causes of an abnormal nutritional status that have been identified include an inadequate intake of protein or calories, an inability to activate the metabolic responses that are needed to achieve nitrogen and protein balance, or the presence of a disease that prevents activation of these metabolic responses or acts to stimulate the breakdown of body protein stores. Three critical metabolic responses to a limited protein intake have been identified: a reduction in the irreversible degradation of amino acids and the degradation of protein breakdown and an increase in protein synthesis in response to a meal. Metabolic acidosis blocks the first two responses and hence contributes to malnutrition in patients with chronic uremia. Other factors that could contribute to malnutrition include an inadequate intake because of anorexia or hormonal imbalances that impair protein turnover. In evaluating CRF patients with malnutrition, the first task is to ensure an adequate intake and to eliminate factors that impair the ability to achieve nitrogen balance.