MR imaging of neurocysticercosis

Magnetic resonance (MR) was performed in 50 patients with neurocysticercosis. Comparison was made with other neuroradiological imaging modalities including CT, myelography, CT ventriculography, and CT myelocisternography. Eighteen patients were found to have intraventricular cysts. In several patients, these were multiple and 22 intraventricular cysts were discovered. Although 4 of the 22 ventricular cysts were missed by MR, T1-weighted images can play a significant role in the early detection of intraventricular cysticercosis cysts, showing the cyst wall (9 of 22), a high intensity mural nodule (6 of 22), and increased signal intensity of the cyst fluid (5 of 22). Cisternal cysts (14 cysts in 10 patients) could be identified; they appear similar to intraventricular cysts, but mural nodules are infrequently seen (1 of 14). Twenty-nine patients had 69 parenchymal cysts. An attempt was made to assess the viability of these parenchymal lesions by matching the CT and MR findings with the Escobar pathologic staging system. Neuroimaging findings seemed compatible with early parenchymal lesions in the vesicular stage in 11 instances. Findings in cases with later stage cysts tend to support the concept that a dying larva provokes pronounced inflammatory reaction in the adjacent brain. Computed tomography remains the superior modality for depicting parenchymal calcifications within dead larvae. A case of a spinal cysticercosis cyst demonstrated with MR (in a patient with extensive intracranial cisternal cysts and a fourth ventricular cyst) is described.     

Lipid metabolism and occurrence of post-percutaneous transluminal coronary angioplasty restenosis: role of cholesteryl ester transfer protein and paraoxonase/arylesterase

Summary.  Plasma lipid metabolic and transfer processes have recently been suggested to play an important role in the development of early restenosis, a major complication of percutaneous transluminal coronary angioplasty (PTCA); in particular, the common variants of genes for cholesteryl ester transfer protein (CETP) and paraoxonase (PONA) have been implicated. We had the opportunity to investigate this question in a large, prospective cohort characterized by quantitative coronary angiography in all subjects. The CETP-Taq IB (intron 1), CETP-Msp I (intron 8), and PONA-Alw I (exon 2) polymorphisms were characterized in a cohort of 779 patients of whom 342 ('cases') had developed restenosis (as defined by > 50% loss of lumen compared with immediate postprocedure results) at repeat angiography at 6 months post PTCA. Selected frequencies for CETP B1 and B2 alleles (absence/presence of Taq IB site) were 0.65 and 0.35 (cases) and 0.65 and 0.35 (controls), respectively; frequencies for CETP M1 and M2 alleles (absence/presence of Msp I site) were 0.20 and 0.80 (cases), 0.21 and 0.79 (controls), respectively; frequencies for PONA A and B alleles (absence/presence of Alw I site) were 0.73 and 0.27 (cases), 0.72 and 0.28 (controls), respectively. All observed genotype frequencies were in Hardy–Weinberg equilibrium. There was no evidence for gene–gene interaction, or an association between genotype and restenosis or degree of lumen loss (adjusted for covariates). Our data, collected in the largest study of its kind so far, indicate that the common variants for CETP and PONA are not associated with incidence of restenosis after PTCA, and are therefore not useful markers for risk assessment.     

HPLC和1HNMR分析确定cis-A-和cis-B-羟甲芬太尼的组成和构型

羟甲芬太尼(1)是一个强效的镇痛剂和高亲和、高选择性的阿片μ受体激动剂。通过HPLC和¹HNMR分析,cis-A-l被确定为由等量的cis-(+)-(3R,4S,2'S)-l和:cis-(—)-(3S,4R,2'R)-1组成的外消旋体,cis-B-l被确定为由等量的cis-(—)-(3R,4S,2'R)-1和cis-(+)-(3S/,4R,2'S)-1组成的外消旋体。     

Effect of postchemotherapy nausea and vomiting on health-related quality of life

The purpose was to measure the effects of postchemotherapy nausea and vomiting (PCNV) on health-related quality of life (HQL) in patients receiving either moderately or highly emetogenic chemotherapy. The study sample consisted of 832 chemotherapy-naive patients with cancer who received either moderately or highly emetogenic chemotherapy as part of multicenter trials of new antiemetics. The patients completed the self-report European Organization for Research and Cancer (EORTC) core Quality of Life Questionnaire (QLQ-C30) before chemotherapy (baseline) and 1 week (day 8) and 2–4 weeks after chemotherapy. They also completed a self-report nausea and vomiting (NV) diary for 5–7 days after chemotherapy. To determine the effects of PCNV on HQL, the change in scores between the baseline and day 8 HQL assessments was calculated for each domain and symptom in the QLQ-C30 and compared in four subgroups of patients: those with both nausea and vomiting, those with nausea but no vomiting, those with no nausea but with vomiting, and those with neither nausea nor vomiting. The group with both nausea and vomiting showed statistically significantly worse physical, cognitive and social functioning, global quality of life, fatigue, anorexia, insomnia and dyspnea as compared to the group with neither nausea nor vomiting (0.0001<P<0.05). Patients with only nausea but no vomiting tended to have less worsening in functioning and symptoms than those having both nausea and vomiting. Increased severity of vomiting (>2 episodes) was associated with worsening of only global quality of life and anorexia as compared with 1–2 episodes of vomiting (0.0001<P<0.01). By 2–4 weeks after chemotherapy all HQL scores had either returned to their baseline levels or were better than baseline. PCNV adversely affects several quality-of-life domains, but patients with only nausea experience less disruption than do those with both nausea and vomiting. Patients with 1–2 episodes of vomiting experience almost the same degree of disruption of HQL as do patients with more than 2 episodes of vomiting.     

Characterization of anti-endothelial cell antibodies in systemic lupus erythematosus (SLE).

IgG anti-endothelial antibodies (AEA), as measured by ELISA or immunoblotting technique could be detected in serum samples of 56 out of 64 patients with SLE (88%) and mainly occurred in monomeric form. AEA were not cell specific, because the binding reactivity was absorbed partially by both fibroblasts and peripheral blood mononuclear cells. No correlation was found between the presence of AEA and anti-nuclear antibodies. Immunoblotting revealed reactivity of AEA against endothelial antigens ranging in size from 15 to 200 kD. AEA titres were significantly higher in patients with joint or skin abnormalities, compared with patients without these abnormalities. A significant correlation was found between nephritis in SLE and the presence of AEA reactivity against endothelial membrane antigens of 38, 41 and 150 kD. These data show that the pattern of AEA reactivity in serum of SLE patients is heterogeneous, and suggest that AEA against a limited number of antigens may be involved in the pathogenesis of nephritis in SLE.     

A sensitive and simplified HPLC analysis for the determination of fluconazol in human plasma

A sensitive and simplified HPLC assay of fluconazol is described. The calibration curve of fluconazol in plasma ranging 0–10 μ g/ml was linear with the correlation coefficients of 0.9900. The limit of detection was 0.3 μ g/ml. The average recovery of the drug was 89.1±9.05%. After oral administration of single dose(150mg) of fluconazol in man, C_max and T_max were 3 μg/ml and 4hr., respectively.     

Apoptosis and apoptosis-associated parameters in relation to tamoxifen exposure in postmenopausal endometrium

Tamoxifen increases endometrial cell proliferation and the incidence of endometrial cancer in postmenopausal women. The purpose of this study was to evaluate apoptosis and apoptosis-related factors in endometrium in relation to tamoxifen exposure. We analyzed benign postmenopausal endometrium from breast cancer patients receiving tamoxifen (n = 35) and from controls (n = 24), and endometrial cancer tissue from tamoxifen-treated breast cancer patients (n = 15) and endometrial cancer from women without tamoxifen exposure (n = 51). Apoptosis was examined morphologically, and the percentage of apoptotic epithelial cells was defined as the apoptotic index. In the benign samples, the presence of apoptotic cells was also evaluated immunohistochemically by the expression of caspase-3 and the monoclonal antibody M30. The expression of Fas, FasL, and Bcl-2 was analyzed in all tissue samples. No differences were observed in the mean apoptotic index in benign endometrium in tamoxifen users (0.17%) versus controls (0.08%), or in tamoxifen-exposed (2.46%) versus nonexposed endometrial cancer (2.28%). However, the ratio of the apoptotic index with the previously reported proliferation index was lower in benign endometrium from tamoxifen users than in controls (0.02 +/- 0.026 vs. 0.05 +/- 0.03, Mann-Whitney U <0.005). In benign endometrium FasL was more frequently expressed in tamoxifen-users than in controls (chi(2) <0.05). We conclude that the apoptosis/proliferation ratio in benign endometrium from tamoxifen users is lower than in controls, indicating that the tamoxifen-induced higher proliferation is not compensated for by increased apoptosis. An imbalance between cell proliferation and apoptosis, and possibly suppression of the antitumor immune response by FasL overexpression in tamoxifen-exposed endometrium might play a role in the development of endometrial cancer in tamoxifen users.     

Prevention of work‐related airway allergies; summary of the advice from the Health Council of the Netherlands

The Health Council of the Netherlands published a report in which the best procedure and method for recommending health‐based occupational exposure limits (OELs) for inhaled allergens were identified by evaluating the scientific state of the art. Many respiratory disorders in the workplace arise from inhalation of substances which can cause allergy. To protect workers against respiratory allergy, various preventive measures are taken, one of them being reduction of exposure by setting legally binding standards. These are based on health‐based OELs that specify a level of exposure to an airborne substance, a threshold level, below which it may reasonably be expected that there is no risk of adverse health effects. The Council is of the opinion that an OEL should prevent against allergic sensitization, as sensitization plays a crucial biological role and is a prerequisite for the development of allergy. Furthermore, the Council considers it most likely that the exposure level below which no allergic sensitization develops for most allergens is so low, that OELs are difficult to set with the current knowledge and technical feasibilities. An alternative approach is to accept exposure, which carries a small predefined risk in developing allergic sensitization. In addition, it is worth considering periodic screening of exposed workers on allergic sensitization, because timely intervention can prevent worse. The feasibility of periodic screening and what else is needed to comply with the most important criteria, should however be judged case‐by‐case.