The Common and Different Neural Bases of Distraction and Reinterpretation: A Meta-Analysis of fMRI Studies.

Distraction and reinterpretation have been recognized as two different tactics of emotion regulation. As a tactic of attention deployment, distraction involves shifting attention to neutral information or performing a secondary task to distract attention from emotion stimuli of the primary task. Reinterpretation, a representative tactic of cognitive change, was defined as changing the meaning of a situation to enhance or reduce its emotional impact. Thus, there are significant differences between the two processes. We wondered if the neural mechanisms underlying distraction and reinterpretation are different. Even though their neural correlates have been widely studied with functional magnetic resonance imaging (fMRI), few studies were conducted to compare the two tactics directly. Here we conducted an activation likelihood estimation (ALE) meta-analyses to investigate the common or different neural bases of distraction and reinterpretation. Moreover, we also used the meta-analytic connectivity modeling (MACM) to identify the emotion regulation network of distraction and reinterpretation. Overall, we found that the left dorsal lateral prefrontal cortex (DLPFC) was consistently activated during distraction and reinterpretation, whereas the left amygdala and inferior frontal gyrus/ventrolateral prefrontal cortex (VLPFC) were specifically activated during reinterpretation alone. The results indicate that the neural basis of distraction and reinterpretation are similar but not identical. The MACM results showed that distraction and reinterpretation share a common emotion regulation network, including the bilateral DLPFC, the dorsal medial prefrontal cortex, the inferior parietal lobule, the insula, the left (pre) supplementary motor area, the left middle temporal gyrus, and the right superior temporal gyrus. However, that network may subserve different functions when adopting various emotion regulation strategies. In addition, we suggest that the emotion regulation network of the left VLPFC may be a specific regulatory network for reinterpretation.

Autosomal deletion/insertion polymorphisms for global stratification analyses and ancestry origin inferences of different continental populations by machine learning methods.

A lot of population data of 30 deletion/insertion polymorphisms (DIPs) of the Investigator DIPplex kit in different continental populations have been reported. Here, we assessed genetic distributions of these 30 DIPs in different continental populations to pinpoint candidate ancestry informative DIPs. Besides, the effectiveness of machine learning methods for ancestry analysis was explored. Pairwise informativeness (In) values of 30 DIPs revealed that six loci displayed relatively high In values (>0.1) among different continental populations. Besides, more loci showed high population-specific divergence (PSD) values in African population. Based on the pairwise In and PSD values of 30 DIPs, 17 DIPs in the Investigator DIPplex kit were selected to ancestry analyses of African, European, and East Asian populations. Even though 30 DIPs provided better ancestry resolution of these continental populations based on the results of PCA and population genetic structure, we found that 17 DIPs could also distinguish these continental populations. More importantly, these 17 DIPs possessed more balanced cumulative PSD distributions in these populations. Six machine learning methods were used to perform ancestry analyses of these continental populations based on 17 DIPs. Obtained results revealed that naïve Bayes manifested the greatest performance; whereas, k nearest neighbor showed relatively low performance. To sum up, these machine learning methods, especially for naïve Bayes, could be used as the valuable tool for ancestry analysis.

Pathological changes induced by phosphine poisoning: a study on 8 children.

Aluminum phosphide (ALP) has been extensively used as an economical and effective insecticide, rodenticide, and fumigant. The active ingredient of ALP is phosphine (PH3), the use of which can lead to accidental inhalation and mass poisoning with high mortality. Exposure to PH3 will give rise to global damage in the human body. This study reviewed 4 fatal accidents including 8 children with PH3 poisoning and aimed to determine the pathological changes that resulted from exposure to PH3 and, secondly, aimed to determine whether oxidative stress was involved in PH3-induced neurotoxicity using histopathological and immunohistochemistry (IHC) methods. After focusing on the pathological changes on the major organs, we found severe damage induced by PH3 in many systems, especially the neurological system, including neuronal, axonal, and vascular injuries as well as oxidative damage with increased expression of 4-hydroxy-2-trans-nonenal (4HNE), 8-hydroxy-2'-deoxyguanosine (8-OH-dG), and 3-nitrotyrosine (3-NT) in the brain, which indicated that oxidative stress was a crucial mechanism for neuronal death in PH3 toxicity. Moreover, we observed severe myocardial and hepatocellular fatty degeneration in the tissues of the heart and liver. We considered that these characteristic changes are a suggestive sign of PH3 poisoning and partly explained the toxic mechanism of PH3 (inhibition of mitochondrial oxidative phosphorylation). We hope that this research could improve the understanding of the toxicity of PH3 in both forensic and clinical practice.

The Water Diffusion of Brain Following Hypoglycemia in Rats - A Study with Diffusion Weighted Imaging and Neuropathologic Analysis.

We established hypoglycemic rat models and divided them into three groups (the sham group, the acute hypoglycemia group and the recovery group). The brain water diffusion was examined using DWI. Thereafter, neuropathologic examinations were performed in order to evaluate the distribution of brain damage. The expression of AQP4 and Caspase3 was also examined using Western blot. We aimed to determine the specific brain regions which were vulnerable to hypoglycemia in relation to the water diffusion and neuropathology. The DWI scanning showed abnormal water diffusion in the cortex, hippocampus and hypothalamus during each stage of hypoglycemia. In the acute hypoglycemia group, the apparent diffusion coefficient (ADC) of the dentate gyrus (DG) and the hypothalamus was increased, while the ADC of the somatosensory cortex (SSc), subcortex and striatum (Str) was decreased. After glucose reperfusion and a 7-day recovery period, most of the hypoglycemia-induced changes in ADC returned to normal, except in the hypothalamus, posterior SSc and DG, which demonstrated increased ADC levels. The lowest AQP4 expression was observed in the cortex of the acute hypoglycemia group. Furthermore, there was increased Caspase3 expression in the hippocampus of the recovery group. The expression of Caspase3 in the hypothalamus was most prominent in the acute hypoglycemia group. Our work revealed that hypoglycemia significantly influenced the water diffusion of the brain. The decrease of AQP4 was associated with the formation of cytotoxic edema in acute hypoglycemia. Hypoglycemia primarily tends to damage the cerebral cortex, hippocampus and hypothalamus and may result in permanent injury to the brain.

Sudden death from an epileptic seizure due to capillary telangiectasias in the hippocampus.

Cerebral capillary telangiectasia (CCT) is a type of vascular malformation that is incidentally encountered in clinical practice. Diseased vessels are small and usually clinically benign over the course of a patient's life. Although most CCT patients are asymptomatic, the situation becomes complicated when trauma is encountered. A case of sudden death due to an epileptic episode after very mild head trauma is reported, including a retrospective study of 12 cases, to remind peers to pay close attention to CCT especially when located in important functional regions of the brain. After immunohistochemical staining and pathological examination, we speculated that the epileptogenic mechanism of CCT may be similar to that of hippocampal sclerosis. As the definite epileptogenic mechanism of CCT in the hippocampus is still elusive, we suggest that more research should be conducted on CCT.