ORIGINAL ARTICLE: Pilot comparison of 18F-fluorocholine and 18F-fluorodeoxyglucose PET/CT with conventional imaging in prostate cancer

Introduction: Conventional imaging (CI) is known to have limitations with respect to staging of patients with primary or relapsed prostate cancer. Positron emission tomography/computed tomography (PET/CT) with ¹⁸F-flurodeoxyglucose (FDG) is also often suboptimal because of low tracer avidity, but ¹⁸F-fluorocholine (FCH) appears to be a promising alternative molecular imaging probe. We report a prospective pilot study of PET/CT comparing both tracers for staging and restaging of patients with prostate cancer. Methods: Sixteen prostate cancer patients were evaluated (7 for staging and 9 for restaging). All patients also underwent CI, comprising at least an abdominopelvic CT and a bone scan. All imaging results and other relevant data were extracted from the imaging reports and medical charts. Results: Based on all imaging-detected disease sites, both FCH-PET/CT and FDG-PET/CT (79%) were more sensitive than CI (14%), with the highest number of sites of nodal and distant disease on FCH PET/CT. FCH-PET/CT alone would have provided sufficient clinical information to form an appropriate management plan in 88% of cases, as compared with 56% for CI. Conclusion: FCH-PET/CT has the potential to impact on the management of patients with prostate cancer significantly more often than CI.     

An 18q- syndrome breakpoint resides between the duplicated serpins SCCA1 and SCCA2 and arises via a cryptic rearrangement with satellite III DNA

The 18q-syndrome is representative of a group of terminal deficiency or macrodeletion syndromes characterized by mental retardation and congenital malformations. To gain insight into the mechanism of chromosomal loss and stabilization in these disorders, we cloned a putative terminal deletion breakpoint from an 18q-syndrome patient. The 18q21.3 breakpoint occurred between two nearly identical serine protease inhibitor (serpin) genes, SCCA1 and SCCA2. Although cytogenetic studies suggested that this chromosomal aberration was formed by a simple terminal deletion, DNA sequence analysis, pulsed- field gel electrophoresis and fluorescence in situ hybridization showed that the breakpoint was contiguous with a 35 bp filler sequence followed by a satellite III DNA-containing telomeric fragment of 475- 1000 kb. This type of satellite III DNA sequence was not detected on the normal chromosome 18, but was highly homologous with types of satellite III DNA sequences normally located on the short arms (p11) of the acrocentric chromosomes and other heterochromatic regions. This DNA sequence analysis suggested that the terminal deficiency in this 18q- syndrome patient arose via illegitimate (non-homologous) recombination. Moreover, these data raise the possibility that a subset of chromosomal aberrations appearing cytogenetically and molecularly as simple terminal truncations or deletions are caused by small (<1000 kb) cryptic rearrangements.      

如何处理疑似IgA过敏性输血反应

输注含血浆的血液制品可能引起不同的过敏反应,包括轻到荨麻疹重至危及生命的喉痉挛或过敏反应。对于后者,鉴别诊断常包括抗-IgA介导的过敏反应,但诊断和治疗的选择是有限的,仅有一些参比实验室才能检测抗IgA,提供IgA阴性的冰冻血浆也是有限的。本文就处理这类临床问题给出“我应该怎么做？”。     

Physician's manual reporting underestimates mortality: evidence from a population-based HIV/AIDS treatment program

Background  

In clinical and cohort research, mortality estimates are often derived from manual reports generated by physicians or electronic reports from vital event registries. We examined the rate of underreporting of deaths by manual methods as compared with electronic reports from a vital event registry.     

广州管圆线虫病诊疗方案

0引言广州管圆线虫病又称嗜酸粒细胞增多性脑膜脑炎或嗜酸粒细胞增多性脑脊髓膜炎.主要是因进食生的或不熟的含有广州管圆线虫幼虫的螺肉而感染,幼虫寄生在中枢神经系统而致病.主要临床表现为脑膜炎、脊髓膜炎、脑炎或脊髓炎,脑脊液内有大量嗜酸性粒细胞.1病原学成虫虫体呈线状     

Genetic testing in familial AD and FTD: Mutation and phenotype spectrum in a Danish cohort

Autosomal dominantly transmitted Alzheimer's disease (AD) and frontotemporal dementia (FTD) are genetically heterogeneous disorders. To date, three genes have been identified in which mutations cause early-onset autosomal dominant inherited AD: APP, PSEN1 , and PSEN2. Mutations in two genes on chromosome 17, the MAPT and the PGRN genes, are associated with autosomal dominant inherited FTD. The aim of this study was to characterize the mutation spectrum and describe genotype-phenotype correlations in families with inherited dementia. The identification of novel mutations and/or atypical genotype-phenotype correlations contributes to further characterizing the disorders. DNA-samples from the 90 index cases from a Danish referral-based cohort representing families with presumed autosomal dominant inherited AD or FTD were screened for mutations in the known genes with sequencing, denaturing high-performance liquid chromatography (DHPLC) and multiplex ligation-dependent probe amplification (MLPA) techniques. Seven presumed pathogenic mutations (two PSEN1 , one PSEN2 , one APP , one MAPT , and two PGRN ) were identified, including a novel PSEN2 mutation (V393M). No dosage aberrations were identified.     

The level of prepulse inhibition in healthy individuals may index cortical modulation of early information processing

This study examined whether baseline PPI levels reflect individual efficiency in tasks associated with routine versus supervisory attentional systems (SAS). PPI and neuropsychological data were collected from 30 healthy male subjects. High PPI was associated with shorter movement times on the 5-choice Reaction Time and shorter Subsequent Thinking Times in the Stockings of Cambridge test. These data suggest that high-PPI status reflects greater efficiency in tasks that engage SAS.     

Increased prepulse inhibition of the acoustic startle response is associated with better strategy formation and execution times in healthy males

Prepulse inhibition (PPI) refers to the attenuation of the amplitude of the startle reflex in response to sudden intense stimuli (pulse) if preceded by a weaker sensory stimulus (prepulse). PPI reflects the ability to filter out irrelevant information in the early stages of processing so that attention can be directed to more salient environmental features. Inhibition at this early stage of information processing appears modulated by the prefrontal cortex in a "top-down" fashion and this may account for the normal inter-individual variability in PPI and in cognitive performance. PPI data were calculated from 82 healthy male subjects who were also tested in problem solving (Stockings of Cambridge; SoC), spatial working memory (SWM) and 5-choice reaction time (RT) tests from the Cambridge Neuropsychological Test Automated Battery. Correlations between PPI scores and cognitive test variables were examined. In addition PPI scores were divided in quartiles which were used as grouping factors in examining cognitive test performance. Compared to individuals in the lowest quartile those in the highest had (a) shorter execution but not reaction times on the 5-choice RT, (b) shorter subsequent but not initial thinking times in the SoC where they also solved more problems correctly with the minimum number of moves, and (c) better strategy but not errors scores in the SWM. Our findings suggest that greater PPI is associated with superior abilities in strategy formation and execution times. We suggest that this is due to more efficient early information processing.