心梗后患者12周康复锻炼后一次递增负荷运动中VO2、HR、%HRmax、RPP、ST、RPE变化及其相互关系

目的:探讨12周运动心脏康复锻炼对心梗后患者(PMI患者)心脏机能的影响。方法:112名男性PMI患者(均进行了12周运动心脏康复锻炼)进行一次递增负荷运动实验(Ⅰ、Ⅱ、Ⅲ、Ⅳ、Ⅴ级负荷跑速分别为1.7、1.7、1.7、2.5、3.5mph;坡度分别为0.5 %、10 %、12 %、14 %,每一级负荷运动3分钟) ,其间记录每级负荷时的VO2、HR、血压和自我用力感觉(RPE) ,计算心率血压乘积(RPP) ,并持续监测12导联心电图(ECG) ,然后对上述指标进行相关分析并建立了用HR和RPE推测VO2和RPP的回归方程。结果:(1)相邻两级负荷间的VO2、HR、RPP、RPE具有显著差异(P<0.01) ;(2)VO2、HR、最大心率百分数( %HRmax)、RPP、ST段水平(ST)和RPE的峰值分别为26.4±7.1ml·kg-1·min-1、126.8±20.3beats·min-1、80.4±12.9 %、209.0±46.3beats·mmHg·100-1、-1.0±0.7mm和14.9±2.1;(3)运动中VO2、HR、%HRmax、RPP、RPE呈高度正相关,它们与ST呈高度负相关(P<0.01或P<0.05) ,建立了用HR和RPE推测VO2和RPP的回归方程。结论:(1)康复锻炼后利用改良Bruce跑台方案进行机能测试有效;(2)12周康复锻炼后,PMI患者进行运动时其强度不宜超过80 %HRmax或RPE不超过15 ;(3)利用本研究建立的预测方程,可在PMI患者康复活动中,根据其心率或RPE变化间接得知其呼吸循环机能的反应和心肌的耗氧状况。     

老年人群亚健康成因及运动处方干预探讨

从当前我国老年退休人群亚健康现状出发,运用文献资料法对老年人群这一特殊群体的亚健康成因进行了探讨与分析,指出社会环境因素、饮食营养因素、生活行为因素、精神心理因素以及自身躯体因素是其产生亚健康状态的主要原因,同时提出了相应的运动干预对策,以其为改善老年人群亚健康状态提供科学依据。     

Randomized phase II – study evaluating EGFR targeting therapy with Cetuximab in combination with radiotherapy and chemotherapy for patients with locally advanced pancreatic cancer – PARC: study protocol [ISRCTN56652283]

Background

Pancreatic cancer is the fourth commonest cause of death from cancer in men and women. Advantages in surgical techniques, radiation therapy techniques, chemotherapeutic regimes, and different combined-modality approaches have yielded only a modest impact on the prognosis of patients with pancreatic cancer. Thus there is clearly a need for additional strategies. One approach involves using the identification of a number of molecular targets that may be responsible for the resistance of cancer cells to radiation or to other cytotoxic agents. As such, these molecular determinants may serve as targets for augmentation of the radiotherapy or chemotherapy response. Of these, the epidermal growth factor receptor (EGFR) has been a molecular target of considerable interest and investigation, and there has been a tremendous surge of interest in pursuing targeted therapy of cancers via inhibition of the EGFR.

Methods/design

The PARC study is designed as an open, controlled, prospective, randomized phase II trial. Patients in study arm A will be treated with chemoradiation using intensity modulated radiation therapy (IMRT) combined with gemcitabine and simultaneous cetuximab infusions. After chemoradiation the patients receive gemcitabine infusions weekly over 4 weeks. Patients in study arm B will be treated with chemoradiation using intensity modulated radiation therapy (IMRT) combined with gemcitabine and simultaneous cetuximab infusions. After chemoradiation the patients receive gemcitabine weekly over 4 weeks and cetuximab infusions over 12 weeks. A total of 66 patients with locally advanced adenocarcinoma of the pancreas will be enrolled. An interim analysis for patient safety reasons will be done one year after start of recruitment. Evaluation of the primary endpoint will be performed two years after the last patient's enrolment.

Discussion

The primary objective of this study is to evaluate the feasibility and the toxicity profile of trimodal therapy in pancreatic adenocarcinoma with chemoradiation therapy with gemcitabine and intensity modulated radiation therapy (IMRT) and EGFR-targeted therapy using cetuximab and to compare between two different methods of cetuximab treatment schedules (concomitant versus concomitant and sequential cetuximab treatment). Secondary objectives are to determine the role and the mechanism of cetuximab in patient's chemoradiation regimen, the response rate, the potential of this combined modality treatment to concert locally advanced lesions to potentially resectable lesions, the time to progression interval and the quality of life.     

Acute barium intoxication and hemodiafiltration

We report a case of severe hypokalemia and flaccid muscle paralysis following a suicide attempt associating the calcium channel blocker amlodipine, the antidepressant fluoxetine and barium carbonate. Despite rapid correction of severe, life-threatening hypokalemia, areflexic quadriplegia persisted, suggesting a direct effect of barium on muscle cells. Continuous veno-venous hemodiafiltration (CVVHDF) was initiated. We determined barium concentration in the urine, plasma, and hemodiafiltrate during CVVHDF. We subsequently calculated the amounts of barium eliminated both by the CVVHDF and the kidneys. CVVHDF triples the measured barium elimination, reduced serum barium half-life by a factor of three, stabilized serum potassium levels, and rapidly improved motor strength, with complete neurological recovery within 24 h. Presentation and treatment of barium intoxication are discussed.     

Lead exposure and children's intelligence: Do low levels of lead in blood cause mental deficit?

It has come to be generally accepted that low levels of lead exposure may result in mental deficit. This causal inference is based on claimed time precedence of the lead exposure and on biological plausibility. The objective of this study is to argue that mental deficit causes pica which causes lead exposure (i.e. to support the theory of reverse causation).

Methodology:

The literature since the 1930s has been interpreted in the light of our own long experience in the investigation of lead exposure in children and adults to support the arguments in favour of reverse causation.

Results:

The arguments for reverse causation are based on: (i) analogy with mental retardation which causes increased lead exposure; (ii) the results of published prospective studies that show a special relationship between blood lead levels at 24 months and intelligence tested later, exactly what would be predicted by the reverse causation theory; and (iii) on an alternative explanation for mental retardation following lead encephalopathy (i.e. that mental retardation following encephalopathy is due to anoxia and not due to a direct destructive effect on the brain neurones). The arguments, which have been proposed for the conventional view, are rejected for the following reasons: (i) none of the prospective studies have found a relationship between cord blood lead levels and intelligence tested later, undermining the argument based on time precedence of lead exposure; and (ii) there is no convincing evidence that lead poisoning, short of encephalopathy, causes mental retardation.

Conclusion:

We believe that the reverse causation hypothesis is a more plausible explanation of the facts.     

Politeal artery entrapment syndrome

Summary We report 15 examples of popliteal artery entrapment syndrome observed in 11 patients. The anatomical causes were as follows: in one case, the popliteal artery presented an aberrant course medially to the medial head of the gastrocnemius muscle. In 5 cases, there was a small fibrous band linking the medial head of the gastrocnemius muscle to the lateral condyle and crossing behind the popliteal artery; in 5 cases this anomaly was also found in association with an abnormally high and/or internal insertion of the medial head of gastrocnemius muscle. In the last 4 cases, there was a muscular insertion anomaly associated with muscular hypertrophy causing arterial compression. Arteriography performed in the 11 patients showed evocative signs of the diagnosis in all cases where the artery was patent. Two popliteal arteries were occluded. CT scan and MRI examination of the popliteal fossa enabled us to define the muscular origin of the popliteal compression. All of the patients were operated upon; two received a reversed saphenous bypass and all of the others were treated by liberation of the popliteal artery and/or vein by a posterior approach. Follow-up in all patients at long term showed good prognosis. All of the patients were able to take up their previous physical activities without sequelae. Our review of the literature, which is based on 374 cases of popliteal artery entrapment observed in 280 patients, made it possible to define the frequency of the various anomalies observed, their symptoms and the different therapeutic possibilities. The multiple anatomical classifications as well as the arterial and muscular embryology are also described.

---

Syndrome de l'artère poplitée piégée. Bases anatomiques et embryologiques, considérations diagnostiques et thérapeutiques à partir d'une expérience de 15 cas et d'une revue de la littérature

Résumé Nous rapportons 15 cas de syndrome de l'a. poplitée piégée observés chez 11 patients. Les causes anatomiques ont été les suivantes : dans un cas l'a. poplitée présentait un trajet aberrant en dedans du chef médial du m. gastrocnémien. Dans cinq cas existait une bandelette fibreuse reliant le chef medial du m. gastrocnémien au condyle latéral du fémur, et croisant l'a. poplitée par en arrière ; dans cinq cas cette anomalie était également présente associée à une insertion anormalement haute et/ou médiale du chef médial du m. gastrocnémien. Dans les quatre derniers cas existait une anomalie d'insertion associée à une hypertrophie musculaire responsable d'une compression artérielle. L'artériographie pratiquée chez les 11 patients a montré des signes évocateurs du diagnostic dans tous les cas où l'artère était perméable. Deux aa. poplitées étaient occluses. L'examen tomodensitométrique et l'IRM des fosses poplitées ont permis de préciser l'origine musculaire de la compression poplitée. Tous les patients ont été opérés ; deux ont bénéficié d'un pontage en v. grande saphène inversée et tous les autres ont été traités par libération de l'a. et/ou de la v. poplitée par voie postérieure. Les suites opératoires ont été simples chez tous les patients y compris à long terme. Tous les patients ont pu reprendre leur activité physique sans séquelle. Notre revue de la littérature qui porte sur 374 pièges poplités observés chez 280 patients permet de préciser la fréquence des différentes anomalies observées, la symptomatologie qu'elles entraînent ainsi que les différentes possibilités thérapeutiques. Les multiples classifications anatomiques ainsi que l'embryologie artérielle et musculaire sont également rappelées.

     

The survival motor neuron protein in spinal muscular atrophy

The 38 kDa survival motor neuron (SMN) protein is encoded by two ubiquitously expressed genes: telomeric SMN (SMN(T)) and centromeric SMN (SMN(C)). Mutations in SMN(T), but not SMN(C), cause proximal spinal muscular atrophy (SMA), an autosomal recessive disorder that results in loss of motor neurons. SMN is found in the cytoplasm and nucleus. The nuclear form is located in structures termed gems. Using a panel of anti-SMN antibodies, we demonstrate that the SMN protein is expressed from both the SMN(T) and SMN(C) genes. Western blot analysis of fibroblasts from SMA patients with various clinical severities of SMA showed a moderate reduction in the amount of SMN protein, particularly in type I (most severe) patients. Immunocytochemical analysis of SMA patient fibroblasts indicates a significant reduction in the number of gems in type I SMA patients and a correlation of the number of gems with clinical severity. This correlation to phenotype using primary fibroblasts may serve as a useful diagnostic tool in an easily accessible tissue. SMN is expressed at high levels in brain, kidney and liver, moderate levels in skeletal and cardiac muscle, and low levels in fibroblasts and lymphocytes. In SMA patients, the SMN level was moderately reduced in muscle and lymphoblasts. In contrast, SMN was expressed at high levels in spinal cord from normals and non- SMA disease controls, but was reduced 100-fold in spinal cord from type I patients. The marked reduction of SMN in type I SMA spinal cords is consistent with the features of this motor neuron disease. We suggest that disruption of SMN(T) in type I patients results in loss of SMN from motor neurons, resulting in the degeneration of these neurons.