In September 2018, heat waves were declared to be a type of natural disaster by the Framework Act on the Management of Disasters and Safety. The present study examined the characteristics of heat waves from the perspectives of meteorological phenomena and health damage. The government’s efforts to minimize the damages incurred by heat waves are summarized chronologically. Furthermore, various issues pertaining to heat waves that are being raised in our society despite the government’s efforts are summarized by analyzing big data derived from reported news and academic articles.

Objectives: Our study aimed to present the distinctive correlates of formal thought disorder in patients with schizophrenia, using the Clinical Language Disorder Rating Scale (CLANG). Methods: We compared clinical characteristics between schizophrenia patients with (n = 84) and without (n = 82) formal thought disorder. Psychometric scales including the CLANG, the Brief Psychiatric Rating Scale (BPRS), the Young Mania Rating Scale (YMRS), the Calgery Depression Scale for Schizophrenia (CDSS) and the Word Fluency Test (WFT) were used. Results: After adjusting the effects of age, sex and total scores on the BPRS, YMRS and WFT, the subjects with disorganized speech presented significantly higher score on the abnormal syntax (p = 0.009), lack of semantic association (p = 0.005), discourse failure (p < 0.0001), pragmatics disorder (p = 0.001), dysarthria (p < 0.0001), and paraphasic error (p = 0.005) items than those without formal thought disorder. With defining the mentioned item scores as covariates, binary logistic regression model predicted that discourse failure (adjusted odds ratio [aOR] = 5.88, p < 0.0001) and pragmatics disorder (aOR = 2.17, p = 0.04) were distinctive correlates of formal thought disorder in patients with schizophrenia. Conclusions This study conducted Clinician Rated Dimensions of Psychosis Symptom Severity (CRDPSS) and CLANG scales on 166 hospitalized schizophrenia patients to explore the sub-items of the CLANG scale independently related to formal thought disorders in schizophrenia patients. Discourse failure and pragmatics disorder might be used as the distinctive indexes for formal thought disorder in patients with schizophrenia.

The tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the tumor necrosis factor family of cytokines. TRAIL selectively induces apoptotic cell death in various tumors and cancer cells, but it has little or no toxicity in normal cells. Agonism of TRAIL receptors has been considered to be a valuable cancer-therapeutic strategy. However, more than 85% of primary tumors are resistant to TRAIL, emphasizing the importance of investigating how to overcome TRAIL resistance. In this report, we have found that nemadipine-A, a cell-permeable L-type calcium channel inhibitor, sensitizes TRAIL-resistant cancer cells to this ligand. Combination treatments using TRAIL with nemadipine-A synergistically induced both the caspase cascade and apoptotic cell death, which were blocked by a pan caspase inhibitor (zVAD) but not by autophagy or a necrosis inhibitor. We further found that nemadipine-A, either alone or in combination with TRAIL, notably reduced the expression of survivin, an inhibitor of the apoptosis protein (IAP) family of proteins. Depletion of survivin by small RNA interference (siRNA) resulted in increased cell death and caspase activation by TRAIL treatment. These results suggest that nemadipine-A potentiates TRAIL-induced apoptosis by down-regulation of survivin expression in TRAIL resistant cells. Thus, combination of TRAIL with nemadipine-A may serve a new therapeutic scheme for the treatment of TRAIL resistant cancer cells, suggesting that a detailed study of this combination would be useful.
Apoptosis* ; Autophagy ; Calcium Channels, L-Type ; Cell Death ; Cytokines ; Down-Regulation* ; Felodipine ; Humans ; Necrosis ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; RNA Interference ; Tumor Necrosis Factor-alpha

O-linked N-acetylglucosamine (O-GlcNAc) represents a key regulatory post-translational modification (PTM) that is reversible and often reciprocal with phosphorylation of serine and threonine at the same or nearby residues. Although recent technical advances in O-GlcNAc site-mapping methods combined with mass spectrometry (MS) techniques have facilitated study of the fundamental roles of O-GlcNAcylation in cellular processes, an efficient technique for examining the dynamic, reciprocal relationships between O-GlcNAcylation and phosphorylation is needed to provide greater insights into the regulatory functions of O-GlcNAcylation. Here, we describe a strategy for selectively identifying both O-GlcNAc- and phospho-modified sites. This strategy involves metal affinity separation of O-GlcNAcylated and phosphorylated peptides, beta-elimination of O-GlcNAcyl or phosphoryl functional groups from the separated peptides followed by dithiothreitol (DTT) conjugation (BEMAD), affinity purification of DTT-conjugated peptides using thiol affinity chromatography, and identification of formerly O-GlcNAcylated or phosphorylated peptides by MS. The combined metal affinity separation and BEMAD approach allows selective enrichment of O-GlcNAcylated peptides over phosphorylated counterparts. Using this approach with mouse brain synaptosomes, we identified the serine residue at 605 of the synapsin-1 peptide, 603QASQAGPGPR612, and the serine residue at 692 of the tau peptide, 688SPVVSGDTSPR698, which were found to be potential reciprocal O-GlcNAcylation and phosphorylation sites. These results demonstrate that our strategy enables mapping of the reciprocal site occupancy of O-GlcNAcylation and phosphorylation of proteins, which permits the assessment of cross-talk between these two PTMs and their regulatory roles.
Acetylglucosamine/*metabolism ; Amino Acid Sequence ; Animals ; Brain/*metabolism ; Chromatography, Affinity ; Glycosylation ; Mice ; Molecular Sequence Data ; Peptides/isolation & purification ; Phosphorylation ; Synapsins/chemistry/*metabolism ; Synaptosomes/*metabolism ; Tandem Mass Spectrometry ; tau Proteins/chemistry/*metabolism