Dopamine transporter density is decreased in parkinsonian patients with a history of manganese exposure: What does it mean?

Manganese (Mn) exposure can cause parkinsonism. Pathological changes occur mostly in the pallidum and striatum. Two patients with a long history of occupational Mn exposure presented with Mn-induced parkinsonism. In one patient, magnetic resonance imaging (MRI) showed findings consistent with Mn exposure, and Mn concentration was increased in the blood and urine. However, this patient's clinical features were typical of idiopathic Parkinson disease (PD). Previous pathological and positron emission tomography studies indicate that striatal dopamine transporter density is normal in Mn-induced parkinsonism, whereas it is decreased in PD. Therefore, we performed [(123)I]-(1r)-2 beta-carboxymethoxy-3beta-(4-iodophenyl)tropane ([(123)I]-beta-CIT) single-photon emission computed tomography. Severe reduction of striatal beta-CIT binding was indicated, which is consistent with PD. We propose three interpretations: (1) the patients have PD, and Mn exposure is incidental; (2) Mn induces selective degeneration of presynaptic dopaminergic nerve terminals, thereby causing parkinsonism; or (3) Mn exposure acts as a risk of PD in these patients. Our results and careful review of previous studies indicate that the axiom that Mn causes parkinsonism by pallidal lesion may be over-simplified; Mn exposure and parkinsonism may be more complex than previously thought. Further studies are required to elucidate the relationship between Mn and various forms of parkinsonism.     

Impact of the supine position versus left horizontal position on colonoscopy insertion: a 2-center,randomized controlled trial

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Memory‐Based Deception Detection: Extending the Cognitive Signature of Lying From Instructed to Self‐Initiated Cheating

From a cognitive perspective, lying can be regarded as a complex cognitive process requiring the interplay of several executive functions. Meta‐analytic research on 114 studies encompassing 3,307 participants (Suchotzki, Verschuere, Van Bockstaele, Ben‐Shakhar, & Crombez, 2017) suggests that computerized paradigms can reliably assess the cognitive burden of lying, with large reaction time differences between lying and truth telling. These studies, however, lack a key ingredient of real‐life deception, namely self‐initiated behavior. Research participants have typically been instructed to commit a mock crime and conceal critical information, whereas in real life, people freely choose whether or not to engage in antisocial behavior. In this study, participants (n = 433) engaged in a trivia quiz and were provided with a monetary incentive for high accuracy performance. Participants were randomly allocated to either a condition where they were instructed to cheat on the quiz (mimicking the typical laboratory set‐up) or to a condition in which they were provided with the opportunity to cheat, yet without explicit instructions to do so. Assessments of their response times in a subsequent Concealed Information Test (CIT) revealed that both instructed cheaters (n = 107) and self‐initiated cheaters (n = 142) showed the expected RT‐slowing for concealed information. The data indicate that the cognitive signature of lying is not restricted to explicitly instructed cheating, but it can also be observed for self‐initiated cheating. These findings are highly encouraging from an ecological validity perspective.     

Synthesis and biodistribution of [18F]FE@CIT, a new potential tracer for the dopamine transporter

In the last decade radiolabeled tropane analogs based on beta-CIT have proven indispensable for the imaging of the dopamine transporter. However, further improvements in their pharmacodynamic and pharmacokinetic features are desirable. An important improvement, yielding in higher affinity to the dopamine transporter (DAT) vs. serotonin transporter (SERT), can be achieved by a simple replacement of the carboxylic methyl ester group in beta-CIT by a fluoroethyl ester. The preparation and ex vivo evaluation of this new beta-CIT-analog ([18F]FE@CIT) is presented here. Precursor and standard were prepared from beta-CIT and analyzed by spectroscopic methods. Yields of precursor and standard preparation were 61% and 42%, respectively. [18F]FE@CIT was prepared by distillation of [18F]bromofluoroethane ([18F]BFE) and reaction with (1R-2-exo-3-exo)8-methyl-3-(4-iodo-phenyl)-8-azabicyclo[3.2.1] octane-2-carboxylic acid. After 10 min at 150 degrees C the product was purified using a C-18 SepPak. The radiosynthesis evinced radiochemical yields of >90% (based on [18F]BFE), the specific radioactivity was >416 GBq/micromol. An average 30 microAh cyclotron irradiation yielded more than 2.5 GBq [18F]FE@CIT. For the ex vivo bioevaluation, 20 male Sprague-Dawley rats were sacrificed at 5, 15, 30, 60, and 120 min after injection. Organs were removed, weighed, and counted. For autoradiographic experiments, transverse brain slices of about 100 microm were prepared. The ex vivo evaluation showed highest brain uptake in striatal regions, followed by thalamus and cerebellum. The highest striatum to cerebellum ratio was 3.73 and the highest thalamus to cerebellum ratio was 1.65. Autoradiographic images showed a good and differentiated uptake in striatal regions with a good target-to-background ratio.     

温度和pH的交互作用对黄绿青霉菌产毒影响

目的在实验室条件下观察温度、pH对黄绿青霉菌（PCV）产毒的影响及其交互作用。方法采用析因实验设计，用察氏培养基培养黄绿青霉菌，二氯甲烷提取黄绿青霉素（CIT）。高效液相色谱法检测CIT毒素含量。结果黄绿青霉菌在高温、低温、酸性及碱性条件下均可产毒，产毒量60．30-336．10μg/g培养基；高温、碱性条件下产毒量较高，是低温条件的2倍以上。结论温度和pH对黄绿青霉菌产毒量有较大影响，且有交互作用。     

黄绿青霉素对心脏毒性损伤作用

目的观察黄绿青霉素（CIT）对离体心肌细胞及大鼠心肌组织结构和功能的损伤。方法电镜检查法观察黄绿青霉素致离体心肌细胞超微结构的改变,并对15mg/（kg·d）CIT喂饲8周的大鼠心肌组织进行病理学观察。结果光镜下CIT处理组大鼠心肌发生变性和坏死,病变呈灶状或条索状分布,有炎性细胞浸润,肌原纤维凝集崩解,部分心肌细胞颗粒变或空泡变性。电镜下,2.5μmol/L CIT组,细胞形状不规则,染色质边集,肌丝明显,胞质内存在脂滴颗粒,线粒体嵴清晰,部分线粒体空泡变性;25μmol/L CIT可使完整的肌细胞结构消失;随剂量增加,毒性作用增强。结论CIT在体内和体外均可引发心肌的变性和坏死。