Molecular docking and kinetic study of transglycosylation reaction for naringenin using amylosucrase from Deinococcus wulumuqiensis

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Diffusion Tensor Tractography Studies on Injured Anterior Cingulum Recovery Mechanisms: A Mini-Review

The cingulum, a major structure in the limbic system, contains the medial cholinergic pathway, which originates from the basalis nucleus of Meynert (Ch 4) in the basal forebrain. The cingulum is involved in various cognitive functions, including memory, attention, learning, motivation, emotion, and pain perception. In this mini-review, 10 studies reporting on recovery mechanisms of injured cinguli in patients with brain injury were reviewed. The recovery mechanisms of the injured anterior cinguli reported in those 10 studies are classified as follows: Mechanism 1, recovery via the normal pathway of the cingulum between the injured cingulum and Ch 4; mechanism 2, recovery through the neural tract between the injured cingulum and the brainstem cholinergic nuclei; mechanism 3, recovery via the lateral cholinergic pathway between the injured cingulum and the white matter of the temporo-occipital lobes; mechanism 4, recovery through the neural tract between the contralesional basal forebrain and the ipsilesional basal forebrain via the genu of the corpus callosum; and mechanism 5, recovery through the neural tract between the injured cingulum and Ch 4 via an aberrant pathway. Elucidation of the recovery mechanisms of injured anterior cinguli might be useful for neurorehabilitation of patients with anterior cingulum injuries. Diffusion tensor tractography appears to be useful in the detection of recovery mechanisms of injured anterior cinguli in patients with brain injury. However, studies on cingulum injury recovery mechanisms are still in the early stages because most of the above studies are case reports confined to a few brain pathologies. Therefore, further studies involving large numbers of subjects with various brain pathologies should be encouraged. In addition, studies on the influencing factors and clinical outcomes associated with each recovery mechanism are warranted

An unusual cause of duodenal perforation due to a lollipop stick

Children have a natural tendency to explore objects with their mouths; this can result in the swallowing of foreign objects. Most ingested foreign bodies pass uneventfully through the gastrointestinal tract. However, some foreign bodies cause obstruction or perforation of the gastrointestinal tract, requiring surgical intervention. Perforation of the gastrointestinal tract may be associated with considerable morbidity and mortality. The most common sites of intestinal foreign body perforation are the ileocecal and rectosigmoid regions. Foreign body perforation of the duodenum is relatively uncommon. We report the first Korean case of duodenal perforation by an ingested 8-cm lollipop stick. Lollipops are popular with the children and fairly accessible to them, as most parents are not aware of their potential harm. Pediatric clinicians should be aware of the risks associated with lollipop stick ingestion. Our report also describes the feasibility and safety of laparoscopic diagnosis and management of pediatric patients with peritonitis induced by the ingestion of foreign bodies

YAF2 promotes TP53-mediated genotoxic stress response via stabilization of PDCD5

AbstractProgrammed cell death 5 (PDCD5) plays a crucial role in TP53-mediated apoptosis, but the regulatory mechanism of PDCD5 itself during apoptosis remains obscure. We identified YY1-associated factor 2 (YAF2) as a novel PDCD5-interacting protein in a yeast two-hybrid screen for PDCD5-interacting proteins. We found that YY1-associated factor 2 (YAF2) binds to and increases PDCD5 stability by inhibiting the ubiquitin-dependent proteosomal degradation pathway. However, knocking-down of YAF2 diminishes the levels of PDCD5 protein but not the levels of PDCD5 mRNA. Upon genotoxic stress response, YAF2 promotes TP53 activation via association with PDCD5. Strikingly, YAF2 failed to promote TP53 activation in the deletion of PDCD5, whereas restoration of wild-type PDCD5WT efficiently reversed the ineffectiveness of YAF2 on TP53 activation. Conversely, PDCD5 efficiently overcame the knockdown effect of YAF2 on ET-induced TP53 activation. Finally, impaired apoptosis upon PDCD5 ablation was substantially rescued by restoration of PDCD5WT but not YAF2-interacting defective PDCD5E4D nor TP53-interacting defective PDCD5E16D mutant. Our findings uncovered an apoptotic signaling cascade linking YAF2, PDCD5, and TP53 during genotoxic stress responses

Genetic and Metabolic Characterization of Insomnia

Insomnia is reported to chronically affect 10∼15% of the adult population. However, very little is known about the genetics and metabolism of insomnia. Here we surveyed 10,038 Korean subjects whose genotypes have been previously profiled on a genome-wide scale. About 16.5% reported insomnia and displayed distinct metabolic changes reflecting an increase in insulin secretion, a higher risk of diabetes, and disrupted calcium signaling. Insomnia-associated genotypic differences were highly concentrated within genes involved in neural function. The most significant SNPs resided in ROR1 and PLCB1, genes known to be involved in bipolar disorder and schizophrenia, respectively. Putative enhancers, as indicated by the histone mark H3K4me1, were discovered within both genes near the significant SNPs. In neuronal cells, the enhancers were bound by PAX6, a neural transcription factor that is essential for central nervous system development. Open chromatin signatures were found on the enhancers in human pancreas, a tissue where PAX6 is known to play a role in insulin secretion. In PLCB1, CTCF was found to bind downstream of the enhancer and interact with PAX6, suggesting that it can probably inhibit gene activation by PAX6. PLCB4, a circadian gene that is closely located downstream of PLCB1, was identified as a candidate target gene. Hence, dysregulation of ROR1, PLCB1, or PLCB4 by PAX6 and CTCF may be one mechanism that links neural and pancreatic dysfunction not only in insomnia but also in the relevant psychiatric disorders that are accompanied with circadian rhythm disruption and metabolic syndrome