Dwarf Novae in the Shortest Orbital Period Regime: I. A New Short Period Dwarf Nova, OT J055717+683226

We report the observation of a new dwarf nova, OT J055717+683226, during its first-ever recorded superoutburst in December 2006. Our observation shows that this object is an SU UMa-type dwarf nova having a very short superhump period of 76.67+/- 0.03 min (0.05324+/-0.00002 d). The next superoutburst was observed in March 2008. The recurrence time of superoutbursts (supercycle) is, hence, estimated to be ~480 d. The supercycle is much shorter than those of WZ Sge-type dwarf novae having supercycles of >~ 10 yr, which are a major population of dwarf novae in the shortest orbital period regime (<~85 min). Using a hierarchical cluster analysis, we identified seven groups of dwarf novae in the shortest orbital period regime. We identified a small group of objects that have short supercycles, small outburst amplitudes, and large superhump period excesses, compared with those of WZ Sge stars. OT J055717+683226 probably belongs to this group.Comment: 14 pages, 11 figures, accepted for publication in PAS

Humeral head histopathological changes in cuff tear arthropathy

Purpose: The aim of this study was to investigate the histopathological changes in the humeral head in cuff tear arthropathy (CTA) compared with those in glenohumeral osteoarthritis (OA) and humeral neck fracture, which served as non-cuff tear controls. Methods: Twenty-three humeral heads extracted at the time of shoulder prosthesis arthroplasty between June 2014 and July 2015 were evaluated in the present study. The diagnoses included four-part humeral neck fracture (n = 4; average age, 85.0 years), glenohumeral OA (n = 4; average age, 71.0 years), and CTA (n = 15; average age, 73.0 years). The humeral heads were evaluated pathologically by hematoxylin and eosin and Safranin-O staining, and the thickness of the articular cartilage was measured. Results: Fibrillation, thinning, and tearing of the cartilage were observed in the superior area of the humeral heads in CTA and glenohumeral OA. In CTA cases, clusters of chondrocytes in the cartilage were observed. Moreover, the thickness of the cartilage layer in the middle of the humeral head was 1.54 ± 0.07, 0.32 ± 0.46, and 2.19 ± 0.50 mm in humeral neck fracture, glenohumeral OA, and CTA, respectively. The cartilage layer in CTA was thicker than that in glenohumeral OA (CTA vs. OA: p < 0.05). Conclusion: OA changes in the superior area of the humeral heads and thickening of the cartilage layer from the middle to the inferior of the humeral heads were confirmed histopathologically, suggesting that simultaneous mechanical and nutritional factors might be contributing to CTA pathogenesis. The current study provided the better understanding of cartilage damage and thickening in CTA. This will help guide treatment options in the setting of CTA

Effect of voltage polarity on oxidation-reduction potential by plasma in water

Use of plasma in water for water treatment and medical treatment is growing and raises expectations of finding advanced functions such as an increase of biological compatibility. In the present study with a focus on the variation of oxidation-reduction potential (ORP), relationships between the electrode polarities of plasma in water and the change of water quality such as conductivity, H2O2 concentration, dissolved hydrogen concentration, pH and ORP were revealed. Similar line spectra of radiation at the electrode tip were observed for each case of positive and negative electrode polarity. The emission intensities of OH (309 nm), Hα (656 nm), and OI (777 nm) for the positive discharge were significantly higher than those for the negative one, though the energy consumption during the discharge period of both cases was nearly the same. Positive electrode polarity was found to be more suitable than negative electrode polarity for increasing dissolved hydrogen gas and hydrogen peroxide. The ORP for the positive polarity decreased from 460 to 45 mV and that for the negative polarity decreased from 460 to 183 mV, although the pH and conductivity were not significantly changed

Senescence-Associated Heterochromatin Foci Suppress γ-H2AX Focus Formation Induced by Radiation Exposure

DNA damage is induced by both endogenous and exogenous factors. Repair of DNA double-strand break (DSB), a serious damage that threatens genome stability, decreases with senescence. However, the molecular mechanisms underlying the decline in DNA repair capacity during senescence remain unclear. We performed immunofluorescence staining for phosphorylated histone H2AX (γ-H2AX) in normal human fetal lung fibroblasts and human skin fibroblasts of different ages after chronic irradiation (total dose, 1 Gy; dose rate, 1 Gy/day) to investigate the effect of cellular senescence and organismal aging on DSB repair. Accumulation of DSBs was observed with cellular senescence and organismal aging, probably caused by delayed DSB repair. Importantly, the formation of γ-H2AX foci, an early event in DSB repair, is delayed with cellular senescence and organismal aging. These results suggest that the delay in γ-H2AX focus formation might delay the overall DSB repair. Interestingly, immediate γ-H2AX foci formation was suppressed in cells with senescence-associated heterochromatin foci (SAHF). To investigate the relationship between the γ-H2AX focus formation and SAHF, we used LiCl to relax the SAHFs, followed by irradiation. We demonstrated that LiCl rescued the delayed γ-H2AX foci formation associated with cellular senescence. This indicates that SAHF interferes with γ-H2AX focus formation and inhibits DSB repair in radiation-induced DSB. Our results suggest that therapeutic targeting of SAHFs have potential to resolve DSB repair dysfunction associated with cellular senescence

Repair Kinetics of DNA Double Strand Breaks Induced by Simulated Space Radiation

Radiation is unavoidable in space. Energetic particles in space radiation are reported to induce cluster DNA damage that is difficult to repair. In this study, normal human fibroblasts were irradiated with components of space radiation such as proton, helium, or carbon ion beams. Immunostaining for &gamma;-H2AX and 53BP1 was performed over time to evaluate the kinetics of DNA damage repair. Our data clearly show that the repair kinetics of DNA double strand breaks (DSBs) induced by carbon ion irradiation, which has a high linear energy transfer (LET), are significantly slower than those of proton and helium ion irradiation. Mixed irradiation with carbon ions, followed by helium ions, did not have an additive effect on the DSB repair kinetics. Interestingly, the mean &gamma;-H2AX focus size was shown to increase with LET, suggesting that the delay in repair kinetics was due to damage that is more complex. Further, the 53BP1 focus size also increased in an LET-dependent manner. Repair of DSBs, characterized by large 53BP1 foci, was a slow process within the biphasic kinetics of DSB repair, suggesting non-homologous end joining with error-prone end resection. Our data suggest that the biological effects of space radiation may be significantly influenced by the dose as well as the type of radiation exposure

Clinical characteristics of pleomorphic carcinoma of the lung

Background: Pleomorphic carcinoma of the lung is a malignant epithelial tumor that contains carcinomatous and sarcomatoid components. Due to its rarity, few studies have been reported, and its clinical and pathological characteristics remain unclear. Method: We retrospectively investigated 22 cases of pleomorphic carcinoma of the lung. Results: Fifteen cases were diagnosed by surgical resection, four by autopsy, and three by transbronchial biopsy. Nineteen patients were male and three were female, and their mean age at diagnosis was 68.3 years (± 10.1). Eighteen were current- or ex-smokers with substantial smoking histories (mean 46.4 pack-years). Sixteen patients had symptoms: hemoptysis and cough were commonly seen. Chest computed tomography (CT) findings revealed that the tumors were quite large (mean diameter 45.3 ± 21.9 mm; range 14-110 mm), and 21 tumors were peripherally located. Positron emission tomography with 18-fluorodeoxy-glucose (FDG-PET) was performed in 12 patients, and the Standardized Uptake Value (SUV) tended to be high (9.44 ± 4.98). In the 15 patients who underwent surgical resection, recurrence was common; systemic metastases were also frequently found. Patients who had received surgical treatment with proper follow-up care survived longer than those who did not undergo surgery. Responses to chemotherapy were generally poor, although one patient exhibited partial response to gefitinib. Conclusions: Pulmonary pleomorphic carcinoma has strong malignant potential with frequent distant metastases, as has already been reported. However, this study demonstrated that surgical treatment and appropriate follow-up therapy might result in better prognoses

Neuroprotective Effect of D-Fructose-1,6-Bisphosphate against beta-Amyloid Induced Neurotoxicity in Rat Hippocampal Organotypic Slice Culture : Involvement of PLC and MEK/ERK Signaling Pathways

D-fructose-1,6-bisphosphate (FBP) is an endogenous intermediate of glycolyticpathway which has potent neuroprotective effect against various neurotoxic insults.This study examined whether FBP could antagonize the neurotoxicity induced byamyloid β-peptide (Aβ) in rat hippocampal organotypic slice cultures, and the possiblemechanism was also explored. Treatment with FBP (concentration ranges from 1.7 mMto 10 mM) significantly decreased the cell death in hippocampal slices in the presence ofAβ at 24h, 48h and 72h, and this neuroprotective effect of FBP against Aβ&#61472; was not in adose-dependent manner, FBP 3.5 mM has better neuroprotective effect than that ofother FBP concentration groups. Treatment with FBP slightly but significantlyincreases the ATP levels in hippocampal slices in the presence of Aβ. However, theincrement of ATP levels was similar among various FBP concentration groups.Neuroprotective effect of FBP 3.5 mM against Aβ induced neurotoxicity inhippocampal slices was attenuated by addition of phospholipase C (PLC) inhibitor,U73122, mitogen activated extracellular signal protein kinase (MEK) inhibitor, U0126,or extracellular signal activated protein kinase (ERK) inhibitor, PD98059 at 24h, 48hand 72h. However, co-treatment with these three kinds of inhibitors did not change theFBP's effect on ATP levels. Our results suggested FBP has neuroprotective effectagainst Aβ induced neurotoxicity in hippocampal slice cultures, and FBP plays role notonly as an alternative energy source, but also a modulator of PLC and MEK/ERKpathways to regulate the cellular response and survival