Comparative Genomics Reveals Adaptation by Alteromonas sp. SN2 to Marine Tidal-Flat Conditions: Cold Tolerance and Aromatic Hydrocarbon Metabolism

Alteromonas species are globally distributed copiotrophic bacteria in marine habitats. Among these, sea-tidal flats are distinctive: undergoing seasonal temperature and oxygen-tension changes, plus periodic exposure to petroleum hydrocarbons. Strain SN2 of the genus Alteromonas was isolated from hydrocarbon-contaminated sea-tidal flat sediment and has been shown to metabolize aromatic hydrocarbons there. Strain SN2's genomic features were analyzed bioinformatically and compared to those of Alteromonas macleodii ecotypes: AltDE and ATCC 27126. Strain SN2's genome differs from that of the other two strains in: size, average nucleotide identity value, tRNA genes, noncoding RNAs, dioxygenase gene content, signal transduction genes, and the degree to which genes collected during the Global Ocean Sampling project are represented. Patterns in genetic characteristics (e.g., GC content, GC skew, Karlin signature, CRISPR gene homology) indicate that strain SN2's genome architecture has been altered via horizontal gene transfer (HGT). Experiments proved that strain SN2 was far more cold tolerant, especially at 5°C, than the other two strains. Consistent with the HGT hypothesis, a total of 15 genomic islands in strain SN2 likely confer ecological fitness traits (especially membrane transport, aromatic hydrocarbon metabolism, and fatty acid biosynthesis) specific to the adaptation of strain SN2 to its seasonally cold sea-tidal flat habitat

Beta-amyloid increases the expression level of ATBF1 responsible for death in cultured cortical neurons

Background: Recently, several lines of evidence have shown the aberrant expression of cell-cycle-related proteins and tumor suppressor proteins in vulnerable neurons of the Alzheimer's disease (AD) brain and transgenic mouse models of AD; these proteins are associated with various paradigms of neuronal death. It has been reported that ATBF1 induces cell cycle arrest associated with neuronal differentiation in the developing rat brain, and that gene is one of the candidate tumor suppressor genes for prostate and breast cancers in whose cells overexpressed ATBF1 induces cell cycle arrest. However, the involvement of ATBF1 in AD pathogenesis is as yet unknown. Results: We found that ATBF1 was up-regulated in the brains of 17-month-old Tg2576 mice compared with those of age-matched wild-type mice. Moreover, our in vitro studies showed that Aβ1-42 and DNA-damaging drugs, namely, etoposide and homocysteine, increased the expression ATBF1 level in primary rat cortical neurons, whereas the knockdown of ATBF1 in these neurons protected against neuronal death induced by Aβ1-42, etoposide, and homocysteine, indicating that ATBF1 mediates neuronal death in response to these substances. In addition, we found that ATBF1-mediated neuronal death is dependent on ataxia-telangiectasia mutated (ATM) because the blockage of ATM activity by treatment with ATM inhibitors, caffeine and KU55933, abolished ATBF1 function in neuronal death. Furthermore, Aβ1-42 phosphorylates ATM, and ATBF1 interacts with phosphorylated ATM. Conclusions: To the best of our knowledge, this is the first report that Aβ1-42 and DNA-damaging drugs increased the ATBF1 expression level in primary rat cortical neurons; this increase, in turn, may activate ATM signaling responsible for neuronal death through the binding of ATBF1 to phosphorylated ATM. ATBF1 may therefore be a suitable target for therapeutic intervention of AD

Analysis of research papers published in the Journal of the Korean Academy of Nursing-focused on research trends, intervention studies, and level of evidence in the research

The number of quantitative studies was greater than that of qualitative studies. There was a slight increase in the number of qualitative studies and studies including elderly populations, which reflects the recent population trend in Korea. More randomized controlled trials with a low risk of bias were needed to support more evidence-based nursing practice. Concerning the low rate of ethical consideration, stricter application of research ethics needs to be encouraged. Conclusion: The findings of this study suggest the recent trends in nursing research and the direction of nursing research and review in the Journal

Phenotyping of rice in salt stress environment using high-throughput infrared imaging

Phenotyping of rice (Oryza sativa L. cv. Donggin) in salt stress environment using infrared imaging was conducted. Results were correlated with the most frequently used physiological parameters such as stomatal conductance, relative water content and photosynthetic parameters. It was observed that stomatal conductance (R2 = –0.618) and relative water content (R2 = –0.852) were significantly negatively correlated with average plant temperature (thermal images), while dark-adapted quantum yield (Fv/Fm, R2 = –0.325) and performance index (R2 = –0.315) were not consistent with plant temperature. Advantages of infrared thermography and utilization of this technology for the selection of stress tolerance physiotypes are discussed in detail

How Does the SST Variability over the Western North Atlantic Ocean Control Arctic Warming over the Barents-Kara Seas?

Arctic warming over the BarentsKara Seas and its impacts on the mid-latitude circulations have been widely discussed. However, the specific mechanism that brings the warming still remains unclear. In this study, a possible cause of the regional Arctic warming over the BarentsKara Seas during early winter (OctoberDecember) is suggested. We found that warmer sea surface temperature anomalies over the western North Atlantic Ocean (WNAO) modulate the transient eddies overlying the oceanic frontal region. The altered transient eddy vorticity flux acts as a source for the Rossby wave straddling the western North Atlantic and the BarentsKara Seas (Scandinavian pattern), and induces a significant warm advection, increasing surface and lower-level temperature over the Eurasian sector of the Arctic Ocean. The importance of the sea surface temperature anomalies over the WNAO and subsequent transient eddy forcing over the WNAO was also supported by both specially designed simple model experiments and general circulation model experiments

A Study of Oral Health Knowledge for Pregnant Women

PURPOSE: This paper examined the relationship between knowledge differences of maternal oral health and of relevant demographic variables. METHODS: Participants included 239 pregnant women who were recruited from Women's Hospital located in B city who agreed to participate in this study. The data were analyzed using descriptive statistics, t-test, ANOVA, Pearson correlation analysis using the SPSS 21.0 program. RESULTS: Maternal knowledge of oral health was moderate level (10.22±2.36). Scores of maternal knowledge of oral health were different according to age, education, occupation, parity, and dental care experience in pregnancy. Level of oral healthcare knowledge was weakly related to age and education. CONCLUSION: Consequently, it is necessary to encourage pregnant women to take part in oral health education program during antenatal care

Recessive C10orf2 mutations in a family with infantile-onset spinocerebellar ataxia, sensorimotor polyneuropathy, and myopathy

Recessive mutations in chromosome 10 open reading frame 2 (C10orf2) are relevant in infantile-onset spinocerebellar ataxia (IOSCA). In this study, we investigated the causative mutation in a Korean family with combined phenotypes of IOSCA, sensorimotor polyneuropathy, and myopathy. We investigated recessive mutations in a Korean family with two individuals affected by IOSCA. Causative mutations were investigated using whole exome sequencing. Electrophysiological analyses and muscle and nerve biopsies were performed, along with magnetic resonance imaging (MRI) of the brain and lower extremities. Compound heterozygous mutations c.1460C>T and c.1485-1G>A in C10orf2 were identified as causative of IOSCA. Skeletal muscle showed mitochondrial DNA (mtDNA) deletions. Both patients showed a period of normal development until 12–15 months, followed by ataxia, athetosis, hearing loss, and intellectual disability. Electrophysiological findings indicated motor and sensory polyneuropathies. Muscle biopsy revealed variations in the size and shape of myofibers with scattered, small, and angulated degenerating myofibers containing abnormal mitochondria; these observations are consistent with myopathy and may be the result of mtDNA deletions. Sural nerve biopsy revealed an axonal neuropathy. High-signal-intensity lesions in the middle cerebellar peduncles were correlated with clinical severity, and MRI of the lower legs was compatible with the hypothesis of length-dependent axonal degeneration. We identified novel compound heterozygous mutations of the C10orf2 gene as the cause of IOSCA with sensorimotor polyneuropathy and myopathy. Signs of motor neuropathy and myopathy were discovered for the first time in IOSCA patients with C10orf2 mutations. These results suggest that the clinical spectrum of IOSCA caused by C10orf2 mutations may be more variable than previously reported. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s10048-014-0405-1) contains supplementary material, which is available to authorized users

Catecholamines May Play an Important Role in the Pathogenesis of Transient Mid- and Basal Ventricular Ballooning Syndrome

The exact pathogenesis of transient mid- and basal ventricular ballooning, a new variant of transient left ventricular (LV) ballooning, remains unknown. We report two cases of transient mid- and basal ventricular ballooning associated with catecholamines. These cases suggest that catecholamine-mediated myocardial dysfunction might be a potential mechanism of this syndrome

Interleukin-2 induces the in vitro maturation of human pluripotent stem cell-derived intestinal organoids.

Human pluripotent stem cell (hPSC)-derived intestinal organoids (hIOs) form 3D structures organized into crypt and villus domains, making them an excellent in vitro model system for studying human intestinal development and disease. However, hPSC-derived hIOs still require in vivo maturation to fully recapitulate adult intestine, with the mechanism of maturation remaining elusive. Here, we show that the co-culture with human T lymphocytes induce the in vitro maturation of hIOs, and identify STAT3-activating interleukin-2 (IL-2) as the major factor inducing maturation. hIOs exposed to IL-2 closely mimic the adult intestinal epithelium and have comparable expression levels of mature intestinal markers, as well as increased intestine-specific functional activities. Even after in vivo engraftment, in vitro-matured hIOs retain their maturation status. The results of our study demonstrate that STAT3 signaling can induce the maturation of hIOs in vitro, thereby circumventing the need for animal models and in vivo maturation