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  • Wiley  (9)
  • 2020-2024  (9)
  • 1
    In: Pediatrics International, Wiley, Vol. 62, No. 5 ( 2020-05), p. 569-575
    Abstract: Group A rotaviruses (RVs) are a major cause of severe gastroenteritis among infants and young children. In Japan, RV vaccines were introduced in 2011, leading to a reduction in severe gastroenteritis cases. Studies are required to assess the effectiveness of the vaccines and their effect on the prevalence of RV genotypes. Methods Fecal samples were collected from outpatients with RV gastroenteritis in a pediatric clinic in Sapporo, Japan, from 2010 to 2016. GPI genotypes were determined using reverse‐transcription polymerase chain reaction. Clinical information and immunization records were obtained from outpatients after 2013. GPI genotypes and clinical features were compared between patients with and without a RV vaccine history. Results In total, 270 cases were genotyped. G1P[8]I1 (Wa‐like G1P[8] ) strains were dominant from 2010 to 2012. G1P[8]I2 (DS‐1‐like G1P[8] ) strains appeared in 2012 and dominated in 2013 to 2015. G2P[4]I2 and G9P[8] I1 strains increased every 3 years (G2P[4]I2: 2011 and 2014, G9P[8] I1: 2010, 2013 and 2016). After the 2013 season, 137 cases were collected, 24 of which were vaccinated. Cases requiring drip infusion were fewer in the vaccination group than in the non‐vaccination group (16.7% vs 52.2%). No patients required hospitalization in the vaccination group compared with 10.6% in the non‐vaccination group. A severe Vesikari score was less common in the vaccination group than in the non‐vaccination group (33.3% vs 78.8%). There was no significant difference in the GPI genotype distribution between the two groups. Conclusion Rotaviruses vaccine effectiveness, regardless of GPI genotype, was confirmed in terms of alleviation of disease severity.
    Type of Medium: Online Resource
    ISSN: 1328-8067 , 1442-200X
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2008621-0
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  • 2
    In: FEBS Open Bio, Wiley, Vol. 11, No. 8 ( 2021-08), p. 2211-2224
    Abstract: There are no human cancer cell lines of external auditory canal origin available for research use. This report describes the establishment of a culture condition for external auditory canal squamous cell carcinoma, derived from human tumor tissue. Successive squamous cell carcinoma colonies were dissociated by trypsin, subcultured, and maintained on a feeder layer (MMC‐TIG‐1‐20), yielding a clonally proliferating cell culture. Two morphological types of colony were observed: (a) densely packed colonies and (b) colonies with indistinct boundaries characterized by cell–cell complexes with fibroblast feeder cells. The SCC‐like characteristics of these cells were evidenced by positivity for p53, SCCA1/2, cytokeratin, and vimentin, and cancer stem cell properties were indicated by positivity for CD44, CD133, Oct3/4, and alkaline phosphatase (ALP). One of the unique properties of cell cultures is their tendency to form steric colonies in vitro on feeder layer cells. In addition, in the presence of fresh macrophages, the cells very slowly transform to break away from colonies as free cells, a process that resembles the epidermal–mesenchymal transition, whereby cell–cell interactions are weakened and migration activity is enhanced. These factors are purported to play a key role in cancer cell metastasis.
    Type of Medium: Online Resource
    ISSN: 2211-5463 , 2211-5463
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2651702-4
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  • 3
    Online Resource
    Online Resource
    Wiley ; 2021
    In:  Alzheimer's & Dementia Vol. 17, No. S9 ( 2021-12)
    In: Alzheimer's & Dementia, Wiley, Vol. 17, No. S9 ( 2021-12)
    Abstract: Establishing preventive and therapeutic methods for Alzheimer's disease (AD) is an urgent issue. Because Vitamin B12(VB12) has a neuroprotective effect on the central nervous system, it has begun to receive attention. Recently, we found that VB12 can suppress β‐amyloid toxicity in vitro. Besides, it has been reported that VB12 might be useful for keeping memory in Mild Cognitive Impairment (MCI). To clarify the effects of VB12 in AD and MCI patients, we examined the effects of the VB12 on cognitive function and regional cerebral blood flow (rCBF). Method We examined 46 participants who consulted to our memory clinic. They were divided into three groups: Alzheimer's disease (AD), mild cognitive impairment (MCI), and healthy controls (HC) based on the National Institute on Aging‐Alzheimer’s Association (NIA‐AA) diagnostic criteria. We used Wechsler Memory Scale‐Revised(WMS‐R) to assess the cognitive function and evaluate what kind of function is degraded. Three‐dimensional stereotactic surface projection(3D‐SSP)was used to quantify the rCBF of hippocampus, thalamus, and callosomarginal regions, which had a well‐established connection with AD. Multiple regression analysis was conducted to examine the correlations among serum VB12, WMS‐R, and rCBF in each group. Result Regarding the correlations between VB12 and memory function, we found that the VB12 was significantly correlated with the WMS‐R scores of visual paired association I/II in the MCI group and the verbal paired associates I in the AD group (all, p 〈 0.05). Besides, there were significant correlations between VB12 and WMS‐R scores of the visual reproduction I, logical memory I, and visual memory span in the HC group (all, p 〈 0.05). Regarding the correlations between VB12 and rCBF, VB12 concentration was significantly correlated with the rCBF of the left hippocampal in the MCI group (all, p 〈 0.05). Neither AD nor HC groups showed significant correlations between rCBF and VB12. Finally, the rCBF of the left hippocampus was positively correlated with visual paired association I/II(all, p 〈 0.05). Conclusion These results suggested that VB12 affects memory function and rCBF, especially in the MCI. Considering the relationship between WMS‐R and rCBF, VB12 may affect the progression of dementia. The early intervention with VB12 can be more effective in AD treatment strategies.
    Type of Medium: Online Resource
    ISSN: 1552-5260 , 1552-5279
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2201940-6
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  • 4
    In: Alzheimer's & Dementia, Wiley, Vol. 16, No. S2 ( 2020-12)
    Abstract: Amyloid β protein (Aβ) molecules that may contribute to Alzheimer's disease (AD) form low molecular weight (LMW‐Aβ), high molecular weight oligomer (HMW‐Aβ) such as protofibrils, and ultimately fibrils. Recent evidence suggests that oxidative stress and plasma membrane damage induced by soluble Aβ oligomers elicit neurotoxicity and play an initiating role in the development of AD pathology. But the precise mechanisms still remain unclear. In this study, we focused on clarifying the detailed mechanism of the HMW‐Aβ neurotoxicity. Method The elution of LMW‐Aβ and HMW‐Aβ was carried out using size exclusion chromatography. SH‐SY5Y cells (Human glioblastoma) were exposed to 5 μM of LMW‐Aβ and HMW‐Aβ for 30 min. To detect cytotoxicity, Aβexposed‐cells were measured mitochondrial activity and release of lactate dehydrogenase. Oxidative stress biomarkers (reactive oxygen species and phospholipid peroxidation of plasma membrane) were assessed. We also assayed intracellular Ca 2+ ([Ca 2+ ] i ) level and membrane fluidity, and membrane electrical resistance by whole‐cell patch‐clamp. Result SH‐SY5Y cells exposed to Aβ oligomers had significantly increased cytotoxicity and oxidative stress compared to untreated cells. The damaging effects of HMW‐Aβ were significantly greater than those of LMW‐Aβ. Exposure of SH‐SY5Y cells to LMW‐Aβ or HMW‐Aβ triggered an elevation in [Ca 2+ ] i . [Ca 2+ ] i levels in SH‐SY5Y cells exposed to HMW‐Aβ rose and maintained high level of [Ca 2+ ] i , while pretreatment with nicardipine and memantine suppressed this continuous rising. Furthermore, both HMW‐Aβ and LMW‐Aβ significantly reduced SH‐SY5Y cell membrane fluidity compared with untreated control cell while, HMW‐Aβ produced a larger decrease in fluidity than did LMW‐Aβ. The resting potential was significantly elevated in SH‐SY5Y cells exposed to HMW‐Aβ compared with untreated control cells and LMW‐Aβ exposed cells and the input resistance was significantly lower following HMW‐Aβ exposure. Conclusion These results suggest that HMW‐Aβchanged the structure of lipid bilayer due to cell membrane phospholipid peroxidation and disrupted the homeostasis of ions across the cell membrane. It was speculated that HMW‐Aβ induced neurotoxicity was induced by membrane structural changes such as the formation of small pores in the cell membrane. Accordingly, we propose that the therapeutic reduction of HMW‐Aβ has important implications for the development of AD therapies.
    Type of Medium: Online Resource
    ISSN: 1552-5260 , 1552-5279
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2201940-6
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  • 5
    In: Reproductive Medicine and Biology, Wiley, Vol. 22, No. 1 ( 2023-01)
    Abstract: Dynamic morphological changes in the chromosome and cytoskeleton occur in mammals and humans during early embryonic development, and abnormalities such as embryonic chromosomal aneuploidy occur when development does not proceed normally. Visualization of the intracellular organelles and cytoskeleton allows elucidation of the development of early mammalian embryos. The behavior of the DNA and cytoskeleton in early mammalian embryos has conventionally been observed by injecting target molecule mRNAs, incorporating a fluorescent substance‐expressing gene, into embryos. In this study, we visualized the chronological behavior of male and female chromosome condensation in mouse embryos, beginning in the two‐pronuclear zygote, through the first division to the two‐cell stage, using fluorescent chemical probes to visualize the behavior of DNA, microtubules, and microfilaments. Method Mouse two‐pronuclear stage embryo were immersed in medium containing fluorescent chemical probes to visualize DNA, microtubules, and microfilaments. Observation was performed with a confocal microscope. Results This method allowed us to observe how chromosome segregation errors in first somatic cell divisions in mouse embryos and enabled dynamic analysis of a phenomenon called lagging chromosomes. Conclusions By applying this method, we can observe any stage of embryonic development, which may provide new insights into embryonic development in other mammals.
    Type of Medium: Online Resource
    ISSN: 1445-5781 , 1447-0578
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2081579-7
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  • 6
    In: Alzheimer's & Dementia, Wiley, Vol. 16, No. S9 ( 2020-12)
    Abstract: Excessive accumulation of β‐amyloid peptide (Aβ) is one of the major mechanisms that cause neuronal death in Alzheimer's disease (AD). We’ve previously shown protofibrils, one of the accumulated Aβ oligomers, are implicated to play a major role. Vitamin B12 (VB12) is an important micronutrient required for brain development and has received attention because of its ability to improve cognitive status in Mild Cognitive Impairment(MCI).However, the protective effects of VB12 against Aβ oligomer‐induced neurotoxicity remain unclear. Recently, we found blood VB12 levels in AD patients are significantly associated with some of the major cognitive functions. Besides, it was associated with left hippocampal blood flow.The purpose of this study was to clarify the mechanism of the protective effect of VB12 against the Aβ oligomer‐induced neurotoxicity. Method Aβ(1‐42) oligomer was eluted using size exclusion chromatography. Neuronal damage was induced in human neuroblastoma cells (SH‐SY5Y) using 5 μM Aβ oligomer. SH‐SY5Y cells were treated with VB12 (50 μM) for 30 min ‐3 hours in combination with Aβ oligomer. Cytotoxicity of Aβ oligomer‐exposed cells was assessed by the 3‐[4,5‐dimethylthiazole‐2‐yl]‐2,5‐diphenyltetrazolium bromide (MTT) and mitochondrial membrane potential (MMP) analyses. Oxidative stress was evaluated by measuring products of reactive oxygen species (ROS), mitochondrial ROS and phospholipid peroxides of plasma cell membranes. Result Aβ oligomers (1, 2.5, 5 and 10 μM) exposure decreased cell viability in a dose‐dependent manner. However, treatment with VB12 significantly recovered the cell viability that was reduced by treatment with Aβ oligomer. MMP significantly decreased with Aβ oligomer and the decrease was significantly suppressed with treatment with VB12, indicating that mitochondria were involved in the neuronal damage induced by Aβ oligomer exposure. Aβ oligomer increased intracellular ROS, mitochondrial ROS and phospholipid peroxides of the plasma membrane, and the increase in Aβ oligomer‐induced oxidative stress was reduced by VB12 treatment. Conclusion These results suggested that the collapse of mitochondria induced by oxidative stress associated with Aβ oligomer exposure was suppressed by treatment with VB12. VB12 may be provided as a therapeutic agent for the prevention of neuronal damage and as a candidate for the treatment of cognitive impairments in AD patients.
    Type of Medium: Online Resource
    ISSN: 1552-5260 , 1552-5279
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2201940-6
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  • 7
    In: Alzheimer's & Dementia, Wiley, Vol. 19, No. S7 ( 2023-06)
    Abstract: Excessive accumulation of amyloid β‐protein (Aβ) is one of the primary mechanisms that leads to neuronal death with phosphorylated tau in the pathogenesis of Alzheimer’s disease (AD). Protofibrils, one of the high‐molecular‐weight Aβ oligomers (HMW‐Aβo), are implicated to be important targets of disease modifying therapy of AD. We previously reported that phenolic compounds such as myricetin inhibit Aβ1‐40, Aβ1‐42, and α‐synuclein aggregations, including their oligomerizations, which may exert protective effects against AD and Parkinson’s disease. The purpose of this study was to clarify the detailed mechanism of the protective effect of myricetin against the neurotoxicity of HMW‐Aβo in SH‐SY5Y cells. Method To assess the effect of myricetin on HMW‐Aβo‐induced oxidative stress, we systematically examined the level of membrane oxidative damage by measuring cell membrane lipid peroxidation, membrane fluidity, and cell membrane potential, and the mitochondrial oxidative damage was evaluated by mitochondrial permeability transition (MPT), mitochondrial reactive oxygen species (ROS), and manganese‐superoxide dismutase (Mn‐SOD), and adenosine triphosphate (ATP) assay in SH‐SY5Y cells. Result Myricetin has been found to increased cell viability by suppression of HMW‐Aβo‐induced membrane disruption in SH‐SY5Y cells, as shown in reducing membrane phospholipid peroxidation and increasing membrane fluidity and membrane resistance. Myricetin has also been found to suppress HMW‐Aβo‐induced mitochondria dysfunction, as demonstrated in decreasing MPT, Mn‐SOD, and ATP generation, raising mitochondrial membrane potential, and increasing mitochondrial‐ROS generation. Conclusion These results suggest that myricetin preventing HMW‐Aβo‐induced neurotoxicity through multiple antioxidant functions may be developed as a disease‐modifying agent against AD.
    Type of Medium: Online Resource
    ISSN: 1552-5260 , 1552-5279
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2201940-6
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  • 8
    In: Acute Medicine & Surgery, Wiley, Vol. 8, No. 1 ( 2021-01)
    Abstract: The Japanese Clinical Practice Guidelines for Management of Sepsis and Septic Shock 2020 (J‐SSCG 2020), a Japanese‐specific set of clinical practice guidelines for sepsis and septic shock created as revised from J‐SSCG 2016 jointly by the Japanese Society of Intensive Care Medicine and the Japanese Association for Acute Medicine, was first released in September 2020 and published in February 2021. An English‐language version of these guidelines was created based on the contents of the original Japanese‐language version. The purpose of this guideline is to assist medical staff in making appropriate decisions to improve the prognosis of patients undergoing treatment for sepsis and septic shock. We aimed to provide high‐quality guidelines that are easy to use and understand for specialists, general clinicians, and multidisciplinary medical professionals. J‐SSCG 2016 took up new subjects that were not present in SSCG 2016 (e.g., ICU‐acquired weakness [ICU‐AW], post‐intensive care syndrome [PICS] , and body temperature management). The J‐SSCG 2020 covered a total of 22 areas with four additional new areas (patient‐ and family‐centered care, sepsis treatment system, neuro‐intensive treatment, and stress ulcers). A total of 118 important clinical issues (clinical questions, CQs) were extracted regardless of the presence or absence of evidence. These CQs also include those that have been given particular focus within Japan. This is a large‐scale guideline covering multiple fields; thus, in addition to the 25 committee members, we had the participation and support of a total of 226 members who are professionals (physicians, nurses, physiotherapists, clinical engineers, and pharmacists) and medical workers with a history of sepsis or critical illness. The GRADE method was adopted for making recommendations, and the modified Delphi method was used to determine recommendations by voting from all committee members. As a result, 79 GRADE‐based recommendations, 5 Good Practice Statements (GPS), 18 expert consensuses, 27 answers to background questions (BQs), and summaries of definitions and diagnosis of sepsis were created as responses to 118 CQs. We also incorporated visual information for each CQ according to the time course of treatment, and we will also distribute this as an app. The J‐SSCG 2020 is expected to be widely used as a useful bedside guideline in the field of sepsis treatment both in Japan and overseas involving multiple disciplines.
    Type of Medium: Online Resource
    ISSN: 2052-8817 , 2052-8817
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2751184-4
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  • 9
    In: Nephrology, Wiley
    Abstract: Type 1 Bartter syndrome causes hypokalaemia and metabolic alkalosis owing to mutation in the SLC12A1 gene. Meanwhile, hypocalcaemia is rare in Bartter syndrome, except in type 5 Bartter syndrome. Herein, we describe two siblings with type 1 Bartter syndrome with recurrent transient severe hypocalcaemia. They each visited our hospital several times with chief complaints of numbness in the limbs, shortness of breath and tetany after stresses such as exercise or fever. Severe hypocalcaemia was also observed with a serum calcium level of approximately 6.0 mg/dL at each visit. The clinical symptoms and abnormalities in laboratory findings quickly improved with rest and intravenous treatment. In a steady state, no severe hypocalcaemia was evident, but serum intact parathyroid hormone (PTH) levels were high. In recent years, a large‐scale study has revealed that type 1 and type 2 Bartter syndrome have high PTH values. In addition, there are reports that these patients develop hypocalcaemia due to PTH resistance. Therefore, our patient was also in a PTH‐resistant state, and hypocalcaemia was thought to be exacerbated by physical stress. It is not well known that Bartter syndrome patients other than those with type 5 suffer from hypocalcaemia. And hypocalcaemia was not detected in normal examinations under steady‐state conditions. Therefore, in patients with type 1 and type 2 Bartter syndrome, severe hypocalcaemia may occur, but may go unnoticed. When following up these patients, the attending physician must keep in mind that such patients are in a PTH‐resistant state and that physical stress can cause severe hypocalcaemia.
    Type of Medium: Online Resource
    ISSN: 1320-5358 , 1440-1797
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2008235-6
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