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Type-II quantum dots (QDs) are emerging as a promising candidate for full color light sources owing to their advantages in achieving full color light by tuning the heterostructures. Despite the recent developments in type-II QDs, the choices of proper materials are limited for the composition of a high-quality QD and it still remains a big challenge to enhance the photoluminescence (PL) quantum yields (QYs) of type-II QDs for light-emitting diode (LED) applications. Here, we develop Cd x Zn 1−x S/ZnSe/ZnS type-II QDs with a maximum quantum yield as high as 88.5%. Time-resolved PL results show that the ZnS shell suppresses non-radiative pathways by passivating the surface of Cd x Zn 1−x S/ZnSe, thus leading to a high QY. Moreover, our results demonstrate that the outer ZnS also benefits the charge injection and radiative recombinations of the Cd x Zn 1−x S/ZnSe. The LED based on green Cd 0.2 Zn 0.8 S/ZnSe/ZnS QDs achieves a current efficiency (CE) of 9.17 cd A −1 , an external quantum efficiency (EQE) of 8.78% and a low turn-on voltage of ∼2.3 V. [ABSTRACT FROM AUTHOR]

This paper is concerned with a parabolic–parabolic Keller–Segel system { u t = ∇ ⋅ ( ∇ u − u ∇ v ) in Ω × ( 0 , T ) , v t = Δ v − v + u in Ω × ( 0 , T ) , ∂ u ∂ ν = ∂ v ∂ ν = 0 on ∂ Ω × ( 0 , T ) , u ( x , 0 ) = u 0 ( x ) ≥ 0 , v ( x , 0 ) = v 0 ( x ) ≥ 0 in Ω in a smoothly bounded domain Ω ⊂ R 2 . Keller and Segel proposed it as a model of aggregation of bacteria, which is mathematically translated as finite-time blowup. A solution ( u , v ) is said to blow up at t = T < + ∞ if lim sup t → T ‖ u ( t ) ‖ L ∞ ( Ω ) = + ∞ . When ( u , v ) blows up at t = T , the blowup is called type I if ‖ u ( t ) ‖ L ∞ ( Ω ) ≤ C ( T − t ) − 1 for t ∈ [ 0 , T ) with some constant C > 0 , and type II otherwise. In spite of motivation of the modeling, it has remained open for the past decades whether or not finite-time blowup occurs frequently in the parabolic–parabolic system. Recently it was shown in [18,19,15] that there exists a large class of radial initial data such that the corresponding solutions blow up in finite time. However they did not give any information on blowup behavior. Blowup rate is one of the greatest concerns in investigation of blowup mechanism. In this paper, we show that each blowup is of type II in the parabolic–parabolic system in radial case. [ABSTRACT FROM AUTHOR]

Osteoarthritis (OA) is a degenerative joint disease affecting millions of people. The degradation and loss of type II collagen induced by proinflammatory cytokines secreted by chondrocytes, such as factor-α (TNF-α) is an important pathological mechanism to the progression of OA. Edaravone is a potent free radical scavenger, which has been clinically used to treat the neuronal damage following acute ischemic stroke. However, whether Edaravone has a protective effect in articular cartilage hasn't been reported before. In this study, we investigated the chondrocyte protective effects of Edaravone on TNF-α induced degradation of type Ⅱ collagen. And our results indicated that TNF-α treatment resulted in degradation of type Ⅱ collagen, which can be ameliorated by treatment with Edaravone in a dose dependent manner. Notably, it was found that the inhibitory effects of Edaravone on TNF-α-induced reduction of type Ⅱ collagen were mediated by MMP-3 and MMP-13. Mechanistically, we found that Edaravone alleviated TNF-α induced activation of STAT1 and expression of IRF-1. These findings suggest a potential protective effect of Edaravone in OA. [ABSTRACT FROM AUTHOR]

Objective To investigate the role of obesity as a risk factor for type II endometrial cancer (EC), as well as the prognostic significance of increasing body mass index (BMI) on survival. Methods A single institution retrospective analysis of 154 type II EC cases from 1987 to 2010 was conducted. Patients were categorized into cohorts by BMI (normal (< 25), overweight (25–29.9), obese class I (30–34.9), and obese class II III (≥ 35)). Descriptive, regression and ANOVA analyses were performed. Kaplan-Meier curves were compared with log rank tests. Results The BMI distribution was 22.8% normal BMI; 24% overweight; 17.5% class I; and 35.7% class II III. The median follow up was 41 months. The median progression-free survival (PFS) was 45.4, 36.0, 35.3 and 42.0 months and overall survival (OS) was 54.7, 44.7, 44.8 and 49.7 months, among the respective groups. There was no association between BMI and PFS (p = 0.71), OS (p = 0.72), or time to recurrence (p = 0.71). There were no differences among the increasing BMI groups compared to normal weight women for the risk of death. Conclusions Our analysis did not reveal any differences in outcomes by BMI group. Our data reveals that obesity is highly prevalent in type II ECs, though obesity has not historically been described as a risk factor. While BMI as a single variable may not be prognostic for survival outcomes, the role of obesity as a risk factor for type II EC should be further investigated, given the increasing prevalence of obesity in type II ECs. [ABSTRACT FROM AUTHOR]

PIP4K2A is a lipid kinase that phosphorylates PtdIns5 P , generating PtdIns4,5 P 2 . Recently, PIP4K2A was identified as a potential target in acute myeloid leukemia cells. The objective of the present study was to investigate the PIP4K2A expression in hematological malignancies and verify the effects of PIP4K2A silencing on proliferation and survival of leukemia cell lines. PIP4K2A was found to be a cytoplasmic and nuclear protein with reduced levels in leukemia cell lines compared to normal leukocytes. PIP4K2A mRNA levels were significantly reduced in bone marrow cells from acute lymphoid leukemia (ALL) patients compared with healthy donors and in myelodysplastic syndromes (MDS) with ≥ 5% compared with < 5% bone marrow blasts. Low PIP4K2A expression (lowest tertile versus 2 higher tertiles) negatively impacted overall survival of MDS patients by univariate analysis. PIP4K2A silencing did not modulate cell proliferation, clonogenicity and apoptosis of HEL and Namalwa leukemia cells. In summary, we characterized the expression of PIP4K2A in a cohort of patients with hematological malignancies and we found that PIP4K2A mRNA expression is downregulated in RAEB-1/RAEB-2 MDS and ALL cells, and PIP4K2A silencing does not modulate cell survival in HEL and Namalwa leukemia cells. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Many studies have examined the impact of older age on tumor recurrence and survival after hysterectomy for patients with endometrioid carcinoma. However, there is paucity of data examining the prognostic significance of age in patients with Type II endometrial carcinoma. The study was conducted to determine the prognostic impact of age in this patient population. Materials and methods: In this Institutional Review Board (IRB)-approved study, our prospectively-maintained database of 1305 patients with endometrial cancer was reviewed. Seventy-two consecutive patients with serous and clear carcinoma 2009 FIGO stages I–II were identified with at least one year follow-up after surgical staging. Patients with mixed histology and those who received preoperative therapy were excluded. All the patients underwent surgical staging from 1989 to 2009. Their medical records were reviewed. The study cohort was divided into two groups based on their age at hysterectomy (≤65 vs. >65). Patient''s demographics, pathologic features and treatment-related factors were compared. The impact of age on recurrence-free survival (RFS), disease-specific survival (DSS) and overall survival (OS) were calculated. Following univariate analysis, multivariate modeling was done using step-wise Cox proportional hazards analysis to assess the impact of age on clinical outcomes after adjusting for various clinical variables. Results: Median follow-up for the study cohort was 45months (range 13–246). Fifty percent of patients received adjuvant platinum-based chemotherapy and/or adjuvant radiation treatment (RT). Thirty-five patients were older than 65years (49%) and 37 were ≤65 (51%). There were no significant differences between the two groups in regard to race (African American vs Caucasian), FIGO stage, number of lymph nodes dissected, lymphovascular space involvement (LVSI), or adjuvant therapy received. There were more clear cell histology in the younger age group (p=0.035). Patients >65years old developed more recurrences with a 5-year RFS of 59% compared to 84% for younger patients (p=0.036). The five-year DSS was not statistically different between the two groups (68% vs. 79%, respectively with p=0.313). 5-year OS was significantly shorter in the elderly patients (58% vs. 78% with p=0.014). On multivariate analysis, the presence of LVSI, not receiving RT and age >65 were independent predictors of worse RFS (p=<0.001, 0.005, and 0.040 respectively). Conclusion: In this study for surgically staged FIGO I–II patients with Type II endometrial carcinoma, age more than 65years is a significant adverse prognostic factor for tumor recurrence. [Copyright &y& Elsevier]

Abstract: Conscious visual perception can fail in many circumstances. However, little is known about the causes and processes leading to failures of visual awareness. In this study, we introduce a new signal detection measure termed subjective discriminability of invisibility (SDI) that allows one to distinguish between subjective blindness due to reduction of sensory signals or to lack of attentional access to sensory signals. The SDI is computed based upon subjective confidence in reporting the absence of a target (i.e., miss and correct rejection trials). Using this new measure, we found that target misses were subjectively indistinguishable from physical absence when contrast reduction, backward masking and flash suppression were used, whereas confidence was appropriately modulated when dual task, attentional blink and spatial uncertainty methods were employed. These results show that failure of visual perception can be identified as either a result of perceptual or attentional blindness depending on the circumstances under which visual awareness was impaired. [Copyright &y& Elsevier]

Abstract: CD95 (Fas/Apo-1)-mediated apoptosis was shown to occur through two distinct pathways. One involves a direct activation of caspase-3 by large amounts of caspase-8 generated at the DISC (Type I cells). The other is related to the cleavage of Bid by low concentration of caspase-8, leading to the release of cytochrome c from mitochondria and the activation of caspase-3 by the cytochrome c/APAF-1/caspase-9 apoptosome (Type II cells). It is also known that the protein synthesis inhibitor cycloheximide (CHX) sensitizes Type I cells to CD95-mediated apoptosis, but it remains contradictory whether this effect also occurs in Type II cells. Here, we show that sub-lethal doses of CHX render both Type I and Type II cells sensitive to the apoptogenic effect of anti-CD95 antibodies but not to chemotherapeutic drugs. Moreover, Bcl-2-positive Type II cells become strongly sensitive to CD95-mediated apoptosis by the addition of CHX to the cell culture. This is not the result of a restraint of the anti-apoptotic effect of Bcl-2 at the mitochondrial level since CHX-treated Type II cells still retain their resistance to chemotherapeutic drugs. Therefore, CHX treatment is granting the CD95-mediated pathway the ability to bypass the mitochondria requirement to apoptosis, much alike to what is observed in Type I cells. [Copyright &y& Elsevier]

Abstract: Glycogen storage disease, type II (GSDII; Pompe disease; acid maltase deficiency) is an autosomal recessive disease caused by mutations of the GAA gene that lead to deficient acid α-glucosidase enzyme activity and accumulation of lysosomal glycogen. Although measurement of acid α-glucosidase enzyme activity in fibroblasts remains the gold standard for the diagnosis of GSDII, analysis of the GAA gene allows confirmation of clinical or biochemical diagnoses and permits predictive and prenatal testing of individuals at risk of developing GSDII. We have developed a clinical molecular test for the detection of GAA mutations based on cycle sequencing of the complete coding region. GAA exons 2–20 are amplified in six independent PCR using intronic primers. The resulting products were purified and sequenced. Preliminary studies using this protocol were conducted with DNA from 21 GSDII-affected individuals from five centers across Canada. In total, 41 of 42 mutations were detected (96.7% detection rate). Mutations spanned intron 1 through exon 19 and included nine novel mutations. Haplotype analysis of recurrent mutations further suggested that three of these mutations are likely to have occurred independently at least twice. Additionally, we report the identification of the c.-32-13T>G GAA mutation in an individual with infantile variant GSDII, despite reports of this mutation being associated almost exclusively with late-onset forms of the disease. The development of a clinical molecular test provides an important tool for the management and counseling of families and individuals with GSDII, and has provided useful information about the GAA mutation spectrum in Canada. [Copyright &y& Elsevier]

Abstract: Matrix vesicles (MVs) are involved in de novo mineral formation by nearly all vertebrate tissues. The driving force for MV mineralization is a nucleational core composed of three principal constituents: (i) amorphous calcium phosphate (ACP), complexed in part with phosphatidylserine (PS) to form (ii) calcium–phosphate–lipid complexes (CPLX), and (iii) annexin A5 (AnxA5), the principal lipid-dependent Ca2+-binding protein in MVs. We describe methods for reconstituting the nucleational core using a biomimetic approach and for analyzing the kinetics of its induction of mineral formation. The method is based on light scattering by the nascent crystallites at 340nm and monitors mineral formation at regular intervals without disturbing the system using an automated plate reader. It yields precise replicate values that typically agree within less than 5%. As with MVs, mineral formation by the synthetic complex follows a sigmoidal pattern; following a quiescent induction period, rapid formation ensues for a limited time, followed by a distinct decline in rate that continues to slow, ultimately reaching a maximal asymptotic value. Key to quantization of mineral formation is the use of first-derivative analysis, which defines the induction time, the rate and the amount of initial mineral formation. Furthermore, using a five-parameter logistic curve-fitting algorithm, the maximal amount of mineral formation can be predicted accurately. Using these methods, we document the dramatic finding that AnxA5 synergistically activates PS–CPLX, transforming it from a very weak nucleator of mineral formation to a potent one. The methods presented should enable systematic study of the effects of numerous other factors thought to contribute to mineral formation. [Copyright &y& Elsevier]

Abstract: Serum IL-18 responses to LPS increase after pretreatment with CpG-containing DNA. Compared to saline-pretreated controls, mice pretreated with CpG for two days produced 20-fold more serum IL-18 when challenged with lipopolysaccharide (LPS). In contrast, IFNγ-deficiency or anti-IFNγ pretreatment reduced CpG-expanded IL-18 responses to LPS by 67 and 83%, respectively. Mice pretreated with either IFNγ or CpG comparably increased LPS-inducible serum IL-18 responses. LPS, compared to challenge with other TLR agonists, was best able to trigger high serum IL-18 levels in CpG-pretreated mice and this response was TLR4-dependent. CpG, compared to pretreatment with other TLR agonists, optimally expanded LPS-induced IL-18 responses that correlated with higher levels of circulating IFNγ levels prior to LPS challenge. High-level serum IL-18 responses were caspase-1-dependent and P2X7 receptor-independent. We conclude that CpG promotes high-level IL-18 synthesis by an IFNγ-dependent and IFNγ-sufficient mechanism in vivo that is optimally triggered by LPS. [Copyright &y& Elsevier]

Abstract: Objectives : According to our previous experience, Type III Nerve-sparing Radical hysterectomy (NSRH) for cervical cancer presented an acceptable urologic morbidity, without compromising radicality. The aim of this study was to compare Type NSRH with other types of RH in terms of incidence of early bladder dysfunctions and perioperative complications. Methods : One hundred and ten patients with cervical cancer were submitted to Type II RH (group 1), Type III NSRH (group 2) and Type III RH (group 3). We assessed the postoperative early bladder function and complications. The follow-up period was 3 months. Results : Group 1 had a significantly shorter duration of the surgery, minor mean blood loss and shorter mean length of postoperative stay when compared to groups 2 and 3. No intraoperative complications were reported in either of the groups. The groups did not differ significantly in terms of GIII/IV morbidity (group 1 = 10%, group 2 = 10% and group 3 = 15%, χ 2, P value: 0.65). Not even they differed in terms of urologic GI–IV morbidity (group 1 = 13%, group 2 = 15% and group 3 = 10%, χ 2, P value = 0.88). Groups 1 and 2 presented a prompt recover of bladder function, significantly different from that of group 3. There was a significant difference between the groups regarding the number of patients discharged with self-catheterism (group 1 = 0; group 2 and group 3 = 11; χ 2, P value ≪ 0.05). Conclusions : The Type III NSRH seems to be comparable to Type II RH and superior to Type III RH in terms of early bladder dysfunctions. [Copyright &y& Elsevier]

Abstract: We have identified a protein, FLJ12673 or FBXO11, that contains domains characteristically present in protein arginine methyltransferases (PRMTs). Immuno-purified protein expressed from one of the four splice variants in HeLa cells and in Escherichia coli exhibited methyltransferase activity. Monomethylarginine, symmetric, and asymmetric dimethylarginine (SDMA, ADMA) were formed on arginine residues. Accordingly, we have designated the protein PRMT9. PRMT9 is the third member of the PRMT family that forms SDMA modifications in proteins. Structurally, this protein is distinct from all other known PRMTs implying that convergent evolution allowed this protein to develop the ability to methylate arginine residues and evolved elements conserved in PRMTs to accomplish this. [Copyright &y& Elsevier]

Abstract: Epithin, a mouse type II transmembrane serine protease, is processed at Gly149 and released from the membrane. Here, we report the identification of an epithin isoform, epithin(Δ), containing a 66 amino acid deletion from the full-length epithin, which is missing the 4th LDLRA domain and the protease activation sequence. This truncated isoform showed the same characteristic N-terminal processing at Gly149 as the full-length form, however, no protease activity was detected. The N-terminal processed epithin(Δ) short form (Epi(Δ)-S) was not released into the medium under conditions in which the processed epithin short form (Epi-S) is released. This type of epithin shedding was also prevented when serine protease inhibitors were added to cells expressing the full-length form. These results strongly suggest that the serine protease activity is involved in the shedding process. The presence of epithin(Δ) message was detected in multiple tissues and its significance is discussed. [Copyright &y& Elsevier]

During ascidian embryogenesis, some mRNAs show clear localization at the posterior-most region. These postplasmic mRNAs are divided into two groups (type I and type II) according to their pattern of localization. To elucidate how these localization patterns are achieved, we attempted to identify the localization elements of these mRNAs. When in vitro synthesized postplasmic mRNAs were introduced into eggs, these mRNAs showed posterior localization similar to the endogenous mRNAs. The posterior localization of these mRNAs was mediated by their 3′ untranslated regions (3′ UTRs), as is the case for several localized Drosophila and Xenopus mRNAs. We identified smaller fragments of the 3′ UTRs of HrWnt-5 and HrPOPK-1 mRNAs (type I) and HrPet-3 mRNA (type II) that were sufficient to direct green fluorescent protein mRNA to the posterior pole. For the localization of HrWnt-5 mRNA, two UG dinucleotide repetitive elements were essential. Motifs similar to these small elements also exist within the HrPOPK-1 mRNA localization element and 3′ UTR of HrZF-1 mRNA, suggesting the conservation of localization elements among type I mRNAs. In contrast, the smallest sequence that suffices for the posterior localization of HrPet-3 (a type II mRNA) has different features from those of type I mRNAs; indeed, it does not have an identifiable critical element. This difference may distinguish type II mRNAs from type I mRNAs. These findings, especially the identification of the small localization element of HrWnt-5 mRNA, provide new insights into the localization of mRNAs during ascidian embryogenesis. [Copyright &y& Elsevier]