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Cyberloafing as a production deviance behavior raises organizational concerns. Unfortunately, it is unknown how to minimize cyberloafing from a bottom-up perspective, particularly different types of cyberloafing. This study draws on the job crafting and dual-process theory to construct a framework for understanding the relationship between task crafting and passive–active cyberloafing, as well as their boundary condition (i.e., supervisor developmental feedback). We adopted a convenient sampling method, following a two-stage sampling with a time interval of 2 weeks. A sample of 614 full-time employed adults were recruited from the online survey. The results showed that: (1) Task crafting was negatively related to passive and active cyberloafing, respectively. (2) The impact of task crafting on passive cyberloafing rather than active cyberloafing was moderated by supervisor developmental feedback, such that task crafting had significant negative relations with passive cyberloafing when supervisor developmental feedback was higher (vs. lower). Overall, our research findings indicate that passive cyberloafing seems more sensitive to the organizational environment than active cyberloafing, thus different types of cyberloafing have different intervention strategies. [ABSTRACT FROM AUTHOR]

Background: We recently encountered a Rhnull phenotype proband within one family in the Chinese population. Rhnull is a rare autosomal recessive disorder characterized by the absence of the Rh antigens on the erythrocyte membrane, resulting in chronic hemolytic anemia. This study described the serological and molecular analysis of a Chinese Rhnull proband and his immediate family. Methods: Red blood cells antigen phenotyping and antibody screening/identification were conducted. RHD, RHCE, and RHAG were analyzed using genomic DNA by polymerase chain reaction and sequence analysis. Results: Serologic tests showed a D–C–E–c–e– phenotype in the proband associated with the suspicion of anti‐Rh29 (titer 16). Molecular analyses showed a new mutation (c.406dupA) in exon 3 of RHAG. This duplication introduced a reading frameshift (p.Thr136AsnfsTer21). The RHAG mutation was found in the homozygous state for the proband and heterozygous state for his parents. Conclusion: We identified a novel RHAG mutation resulting in the Rhnull phenotype of the regulator type. Inheritance of the novel allele was shown by family study. [ABSTRACT FROM AUTHOR]

Aim: To evaluate the effectiveness of a professional identity promotion strategy (PIPS) on nursing students' professional identity and resilience. Methods: This study was a quasi‐experimental study with a random cluster sample of 103 sophomore undergraduate nursing students. One hundred students answered the questionnaires at both baseline and follow‐up (51 of 53 in the intervention group and 49 of 50 in the control group). Intervention and control groups underwent 5 months PIPS and standard professional education from May 2 to September 27, respectively. Participants completed the professional identity questionnaire for nursing students (PIQNS) and Connor–Davidson resilience scale (CD‐RISC). Data were collected at baseline (T0), after the intervention (T1) and 3 months after the intervention (T2), and analyzed using the Chi‐squared test, Fisher's exact test, and repeated‐measures analysis of variance. Results: There were no significant differences between the two groups (p >.05) regarding demographic questions, professional identity, or resilience at baseline (p >.05). Significant differences were found in professional identity between groups (p <.001), measurement times (p =.026), and in the interaction between groups and measurement times (p =.018) from T0 to T2. Significant differences were found in resilience between groups (p <.001), measurement times (p =.007), and in the interaction between groups and measurement times (p =.035) from T0 to T2. Conclusions: The PIPS program improved nursing students' professional identity and resilience. Further long‐term effectiveness of the program needs to be tested with implementation through various forms of mobile technology. [ABSTRACT FROM AUTHOR]

Background: This systematic review and meta-analysis seek to evaluate the prevalence of nodal disease in rectal cancer patients with pathological complete responses (pCR) after neoadjuvant chemoradiotherapy (ypT0N+). Methods: This study conformed to the PRISMA guidelines. A search was performed on major databases to identify relevant articles. Meta-analyses of pooled proportions were performed on rectal cancer with pCR and ypT0N+. Meta-regression was undertaken to identify sources of heterogeneity, and the Newcastle-Ottawa Scale (NOS) was employed to assess the risk of bias. Results: A total of 18 studies were included, totaling 7568 patients. The overall risk of bias was low, since all studies scored 6 and above out of 9 on the NOS. Preoperatively, the pooled proportions of patients with T3/T4 tumors and clinically positive nodal disease were 84.08% (95% CI 74.19 to 91.99%) and 52.14% (95% CI 35.02 to 69.00%) respectively. The prevalence of pCR in the whole pool was 18.52% (95% CI 13.31 to 24.35%; I2 = 93.85%; P = 0.00), and meta-regression showed a significantly negative relationship with patient age (β = − 0.03, 95% CI − 0.03 to − 0.02; P = 0.00). The pooled prevalence of ypT0N+ was 4.61% (95% CI 2.41 to 7.28%; I2 = 52.27%; P = 0.01), and meta-regression demonstrated a significantly positive relationship with male gender (β = 1.06, 95% CI 1.00 to 1.12; P = 0.04). Conclusion: There is a small risk of ypN+ in patients with pCR after neoadjuvant CRT and surgery for rectal cancer. However, further research is warranted to establish these findings and to identify predictive factors for this specific group of patients. [ABSTRACT FROM AUTHOR]

In the Drosophila melanogaster compound eye, myosin-5 (DmM5) plays two distinct roles in response to light stimulation: transport of pigment granules to the rhabdomere base to decrease light exposure and transport of rhodopsin-bearing vesicles to the rhabdomere base to compensate for the rhodopsin loss during light exposure. However, little is known of how the motor function of DmM5 is regulated at the molecular level. In the present study, we overexpressed DmM5 in Sf9 insect cells and investigated its regulation using purified proteins. We found that the actin-activated ATPase activity of DmM5 is significantly lower than that of the truncated DmM5 having the C-terminal globular tail domain (GTD) deleted, indicating that the GTD is the inhibitory domain. The actin-activated ATPase activity of DmM5 is significantly activated by micromolar levels of calcium. DmM5 associates with pigment granules and rhodopsin-bearing vesicles through cargo-binding proteins Lightoid (Ltd) and dRab11 respectively. We found that GTP-bound dRab11, but not Ltd, significantly activates DmM5 actin-activated ATPase activity. Moreover, we identified Gln1689 in the GTD as the critical residue for the interaction with dRab11 and activation of DmM5 motor function by dRab11. Based on those results, we propose that DmM5-dependent transport of pigment granules is directly activated by light-induced calcium influx and the DmM5-dependent transport of rhodopsin-bearing vesicle is activated by active GTP-bound dRab11, whose formation is stimulated by light-induced calcium influx. [ABSTRACT FROM AUTHOR]

Wilson disease is an inherited disorder of excessive copper accumulation. The commonly used drug d -penicillamine (PA) or trientine both cause a high incidence (10–50%) of neurological worsening, which rarely occurs with tetrathiomolybdate (TM) treatment. To investigate the mechanisms of neurologic deterioration after the initiation of chelation therapy, brain hydroxyl radical and free copper were assessed in vivo in this study. On days 3, 7, 14, and 21 after PA or TM administration, striatal hydroxyl radical levels of both TX mice and controls were assessed by terephthalic acid (TA) combined with microdialysis and high-performance liquid chromatography (HPLC). Within the same microdialysis samples, free copper was measured by inductively coupled plasma mass spectrometry (ICP-MS). The results showed that both hydroxyl radical and free copper markedly increased in the striatum of TX mice during PA administration but were not elevated when administering TM. These results suggested that the further increased free copper in the brain and oxidative stress caused by some chelators might contribute to the neurological deterioration. [ABSTRACT FROM AUTHOR]

Class XIX myosin (Myo19) is a vertebrate-specific unconventional myosin, responsible for the transport of mitochondria. To characterize biochemical properties of Myo19, we prepared recombinant mouse Myo19-truncated constructs containing the motor domain and the IQ motifs using the baculovirus/Sf9 expression system. We identified regulatory light chain (RLC) of smooth muscle/non-muscle myosin-2 as the light chain of Myo19. The actin-activated ATPase activity and the actin-gliding velocity of Myo19-truncated constructs were about one-third and one-sixth as those of myosin-5a, respectively. The apparent affinity of Myo19 to actin was about the same as that of myosin-5a. The RLCs bound to Myo19 could be phosphorylated by myosin light chain kinase, but this phosphorylation had little effect on the actin-activated ATPase activity and the actin-gliding activity of Myo19-truncated constructs. Using dual fluorescence-labeled actin filaments, we determined that Myo19 is a plus-end-directed molecular motor. We found that, similar to that of the high-duty ratio myosin, such as myosin-5a, ADP release rate was comparable with the maximal actin-activated ATPase activity of Myo19, indicating that ADP release is a rate-limiting step for the ATPase cycle of acto-Myo19. ADP strongly inhibited the actin-activated ATPase activity and actin-gliding activity of Myo19-truncated constructs. Based on the above results, we concluded that Myo19 is a high-duty ratio molecular motor moving to the plus-end of the actin filament. [ABSTRACT FROM AUTHOR]

Magnesium (Mg2+), an essential structural component of chlorophyll, is absorbed from the soil by roots and transported to shoots to support photosynthesis in plants. However, the molecular mechanisms underlying root-to-shoot Mg2+ translocation remain largely unknown. We describe here the identification of four plasma membrane (PM)-localized transporters, named Mg2+ release transporters (MGRs), that are critical for root-to-shoot Mg transport in Arabidopsis. Functional complementation assays in a Mg2+-uptake-deficient bacterial strain confirmed that these MGRs conduct Mg2+ transport. PM-localized MGRs (MGR4, MGR5, MGR6, and MGR7) were expressed primarily in root stellar cells and participated in the xylem loading step of the long-distance Mg2+ transport process. In particular, MGR4 and MGR6 played a major role in shoot Mg homeostasis, as their loss-of-function mutants were hypersensitive to low Mg2+ but tolerant to high Mg2+ conditions. Reciprocal grafting analysis further demonstrated that MGR4 functions in the root to determine shoot Mg2+ accumulation and physiological phenotypes caused by both low- and high-Mg2+ stress. Taken together, our study has identified the long-sought transporters responsible for root-to-shoot Mg2+ translocation in plants. Plants deliver Mg2+ to shoots, which is crucial for chloroplast structure and photosynthesis. In this study, the authors have identified four plasma membrane-localized Mg2+ release transporters (MGRs) that can load Mg2+ into the xylem and thus determine shoot Mg2+ accumulation in Arabidopsis. [ABSTRACT FROM AUTHOR]

Abstract: Highly active, hierarchical zeolite ZSM-5 aggregates have been prepared in a one-step synthesis using alkanolamine as single template. The effects of SiO2/Al2O3, pH and H2O/SiO2 on the aggregate morphology of the ZSM-5 nanocrystals were investigated. The obtained aggregate zeolites characterized by SEM, TEM and BET possessed significant textual porosity (up to 0.22 cm3/g), which could be tuned by the number of substituents in the alkanolamine molecules and the amount of aluminum in the synthetic mixtures. These zeolite aggregates showed high activities for Friedel–Crafts alkylations and may curtail the filtration difficulties during the synthesis and applications to some extent. [Copyright &y& Elsevier]

By incorporating psychopathology and subjective well-being (SWB), the dual-factor model of mental health (DFM) can comprehensively measure psychological health. We examined the utility of the DFM among 1,293 Chinese adolescents (Grades 7–12). Furthermore, we examined the dynamics of mental health group membership via a two-wave longitudinal study of 531 students. SWB, psychopathology, affective self-regulatory efficacy, academic self-efficacy, and academic emotions were measured via self-report scales. Mental health group membership was determined according to combinations of high or low SWB and high or low psychopathology. The DFM was supported by our identification of its four constituent groups (i.e. complete mental health, vulnerable, troubled, and symptomatic but content). Significant group differences were found in affective self-regulatory efficacy, academic self-efficacy, and academic emotions, with clear contrasts observed between adolescents with complete mental health and their vulnerable peers, as well as between troubled adolescents and their symptomatic but content peers. Moreover, youth with complete mental health demonstrated the highest stability and troubled youth the lowest, whereas vulnerable youth had the highest rates of transitioning into both the complete mental health and troubled groups. Implications for practice are explored within the context of screening and intervention. [ABSTRACT FROM AUTHOR]

Objectives: Mutations in RAB39B have been reported as a potential cause of X-linked Parkinson's disease (PD), a rare form of familial PD. We conducted a genetic analysis on RAB39B to evaluate whether RAB39B mutations are related to PD in the Chinese population.Methods: In this study, 2 patients from an X-linked juvenile parkinsonism pedigree were clinically characterized and underwent whole-exome sequencing. A comprehensive screening for RAB39B mutations in 505 sporadic patients with PD and 510 healthy controls in a Chinese population was also performed.Results: A novel mutation, c. 536dupA (p.E179fsX48), in RAB39B was identified in the juvenile parkinsonism pedigree. Brain MRI and CT scans in the 2 patients revealed calcification within the bilateral globus pallidus. No other potentially disease-causing RAB39B mutations were found in sporadic PD patients and controls.Conclusions: X-linked juvenile parkinsonism could be caused by a RAB39B mutation, and basal ganglia calcification may be a novel clinical feature of RAB39B-related parkinsonism. © 2016 International Parkinson and Movement Disorder Society. [ABSTRACT FROM AUTHOR]

The motor function of vertebrate myosin-5a is inhibited by its tail in a Ca2+-dependent manner. We previously demonstrated that the calmodulin (CaM) bound to the first isoleucine-glutamine (IQ) motif (IQ1) of myosin-5a is responsible for the Ca2+-dependent regulation of myosin-5a. We have solved the crystal structure of a truncated myosin-5a containing the motor domain and IQ1 (MDIQ1) complexedwith Ca2+-bound CaM (Ca2+-CaM) at 2.5-Å resolution. Comparedwith the structure of the MD-IQ1 complexed with essential light chain (an equivalent of apo-CaM), MD-IQ1/Ca2+-CaM displays large conformational differences in IQ1/CaM and little difference in the motor domain. In the MD-IQ1/Ca2+-CaM structure, the N-lobe and the C-lobe of Ca2+-CaM adopt an open conformation and grip the C-terminal and the N-terminal portions of the IQ1, respectively. Remarkably, the interlobe linker of CaMin IQ1/Ca2+-CaM is in a position opposite that in IQ1/apo-CaM, suggesting that CaM flip-flops relative to the IQ1 during the Ca2+ transition. We demonstrated that CaM continuously associates with the IQ1 during the Ca2+ transition and that the binding of CaM to IQ1 increases Ca2+ affinity and substantially changes the kinetics of the Ca2+ transition, suggesting that the IQ1/CaM complex functions as an intact Ca2+ sensor responding to distinct calcium signals. [ABSTRACT FROM AUTHOR]

Mesoporous silica materials were synthesized using tetraеthoxysilane as precursor and liquid crystals formed in aqueous mixtures of cetyl trimethyl ammonium bromide (CTAB) and sodium dodecyl sulfate (SDS) as templates, without and with the addition of NaBr or NaSO. For this purpose, the formation of liquid crystals as a function of the ratio of CTAB and SDS under different conditions was studied. It was found that liquid crystals formed in the mixed system of CTAB and SDS at certain mixing ratios are well-structured templates for the synthesis of mesoporous silicas. The synthesized silica materials were characterized by transmission electron microscope and nitrogen adsorption/desorption analysis. The pore size of mesoporous silicas could be controlled between 3 to 6 nm by simply changing the concentration of NaBr in solution. The mesoporous silicas exhibited lamellar structure and the order of structural arrangement was promoted with addition of NaBr. However, addition of NaSO led to ink-bottle type pores of mesoporous silica with a narrow pore size distribution of around 2 nm and a higher specific surface area of 610 m g. [ABSTRACT FROM AUTHOR]

This study aimed to explore the value of a real-time comparative observation method using contrast-enhanced ultrasound (CEUS) for discriminating between bronchial and pulmonary arterial phases in diagnosing lung diseases. Forty-nine patients with 50 pulmonary lesions (45 peripheral lesions and five central lesions with obstructive atelectasis, including 36 malignant tumors, five tuberculomas, four inflammatory pseudotumors and five pneumonia lesions) detected via computed tomography and visible on ultrasonography were enrolled in this study. The arterial phases were determined by comparing contrast agent arrival time (AT) in the peripheral lung lesion with that in adjacent lung tissue, referred to as a real-time comparative observation method. Detection rates of this observation method were 100% (50/50) for pulmonary arterial phase and 88% (44/50) for bronchial arterial phase. Using the instrument's built-in graphing and analysis software, a time-intensity curve was constructed based on a chosen region of interest within the lesion where enhancement was the most obvious. Commonly used perfusion indicators in CEUS, such as AT, time-to-peak and peak intensity, were obtained from the time-intensity curve. Percutaneous puncture biopsies were performed under ultrasound guidance, and specimens of all 50 lesions were examined pathologically. AT was significantly shorter in patients with pneumonia than in those with malignant tumors or chronic inflammation (p < 0.05), whereas no difference was seen between those with malignant tumors and those with chronic inflammation. No significant differences in time-to-peak or peak intensity were seen among those with various lung diseases (p > 0.05). This is the first description of a real-time comparative observation method using CEUS for determining the arterial phases in the lungs. This method is accurate, simple to perform and provides a direct display. It is expected to become a practical and feasible tool for diagnosing lung diseases. [ABSTRACT FROM AUTHOR]

The tail-inhibition model is generally accepted for the regulation of myosin-5a motor function. Inhibited myosin-5a is in a folded conformation in which its globular tail domain (GTD) interacts with its head and inhibits its motor function, and high Ca2+ or cargo binding may reduce the interaction between the GTD and the head of myosin-5a, thus activating motor activity. Although it is well established that myosin-5a motor function is regulated by Ca2+, little is known about the effects of cargo binding. We previously reported that melanophilin (Mlph), a myosin-5a cargo-binding protein, is capable of activating myosin-5a motor function. Here, we report that Mlph-GTBDP, a 26 amino-acid-long peptide of Mlph, is sufficient for activating myosin-5a motor function. We demonstrate that Mlph-GTBDP abolishes the interaction between the head and GTD of myosin-5a, thereby inducing a folded-to-extended conformation transition for myosin-5a and activating its motor function. Mutagenesis of the GTD shows that the GTD uses two distinct, non-overlapping regions to interact with Mlph-GTBDP and the head of myosin-5a. We propose that the GTD is an allosteric protein and that Mlph allosterically inhibits the interaction between the GTD and head of myosin-5a, thereby activating myosin-5a motor function. [ABSTRACT FROM AUTHOR]

Myosin 5a is as yet the best-characterized unconventional myosin motor involved in transport of organelles along actin filaments. It is well-established that myosin 5a is regulated by its tail in a Ca2+-dependent manner. The fact that the actin-activated ATPase activity of myosin 5a is stimulated by micromolar concentrations of Ca2+ and that calmodulin (CaM) binds to IQ motifs of the myosin 5a heavy chain indicates that Ca2+ regulates myosin 5a function via bound CaM. However, it is not known which IQ motif and bound CaM are responsible for the Ca2+-dependent regulation and how the head-tail interaction is affected by Ca2+. Here, we found that the CaM in the first IQ motif (IQ1) is responsible for Ca2+ regulation of myosin 5a. In addition, we demonstrate that the C-lobe fragment of CaM in IQ1 is necessary for mediating Ca2+ regulation of myosin 5a, suggesting that the C-lobe fragment of CaM in IQ1 participates in the interaction between the head and the tail. We propose that Ca2+ induces a conformational change of the C-lobe of CaM in IQ1 and prevents interaction between the head and the tail, thus activating motor function. [ABSTRACT FROM AUTHOR]

Alarmins S100A8 and S100A9 are endogenous molecules released in response to environmental triggers and cellular damage. They are constitutively expressed in immune cells such as monocytes and neutrophils and their expression is upregulated under inflammatory conditions. The molecular mechanisms that regulate inflammatory pathways in tendinopathy are largely unknown therefore identifying early immune effectors is essential to understanding the pathology. Based on our previous investigations highlighting tendinopathy as an alarmin mediated pathology we sought evidence of S100A8 & A9 expression in a human model of tendinopathy and thereafter, to explore mechanisms whereby S100 proteins may regulate release of inflammatory mediators and matrix synthesis in human tenocytes. Immunohistochemistry and quantitative RT-PCR showed S100A8 & A9 expression was significantly upregulated in tendinopathic tissue compared with control. Furthermore, treating primary human tenocytes with exogenous S100A8 & A9 significantly increased protein release of IL-6, IL-8, CCL2, CCL20 and CXCL10; however, no alterations in genes associated with matrix remodelling were observed at a transcript level. We propose S100A8 & A9 participate in early pathology by modulating the stromal microenvironment and influencing the inflammatory profile observed in tendinopathy. S100A8 and S100A9 may participate in a positive feedback mechanism involving enhanced leukocyte recruitment and release of pro-inflammatory cytokines from tenocytes that perpetuates the inflammatory response within the tendon in the early stages of disease. [ABSTRACT FROM AUTHOR]