Research on managing post-80s employees In China

More and more young employees who were born after1980 move into the labor market after 2000. They started to become an important part of human resources in various organizations. Meanwhile, the management problems emerging due to the new generation employees increased much research interest by the academic ground and the whole society. In industrial times, the employee management emphasizes on managing the employees instead of developing them. Nowadays organizations and managers have been paying more attention to inner factors of human beings, such as their psychological and behavior nature. In recent years, the career development model has been changing with the innovation of organizational structure and traditional labor relations. Traditional employment relationship has crumbled, while the employees' attitude to the organization and career development has transformed. The post-80s generation employees are no longer loyal to their companies but are loyal to their own career development. The enterprises which aim to get loyalty from their employees have to build up equal, respectful and reliable partnership with the employees, providing a promising platform and leading them to be loyal to the organization. Research on post-80s and 90s generation employees has been immature and there is no system structure on it. The thesis intends to define the characters of the post-80s and 90s in the workplace, and build a framework and analyses of the phenomenon. Multiple methods such as questionnaire, documentation and qualitative have been used to study the problem in this thesis and it has given sound research conclusions and management advice for the companies to manage post-80s and 90s generation employees

IκB Kinase β Regulates Epithelium Migration during Corneal Wound Healing

The IKKβ is known to regulate transcription factor NF-κB activation leading to inflammatory responses. Recent gene knockout studies have shown that IKKβ can orchestrate local inflammatory responses and regulate homeostasis of epithelial tissues. To investigate whether IKKβ has an intrinsic role in epithelial cells, we established an in vivo system in the immune privileged corneal epithelium. We generated triple transgenic Krt12rtTA/rtTAt/tet-O-Cre/IkkβF/F (IkkβΔCE/ΔCE) mice by crossing the Krt12-rtTA knock-in mice, which express the reverse tetracycline transcription activator in corneal epithelial cells, with the tet-O-Cre and IkkβF/F mice. Doxcycline-induced IKKβ ablation occurred in corneal epithelial cells of triple transgenic IkkβΔCE/ΔCE mice, but loss of IKKβ did not cause ocular abnormalities in fetal development and postnatal maintenance. Instead, loss of IKKβ significantly delayed healing of corneal epithelial debridement without affecting cell proliferation, apoptosis or macrophage infiltration. In vitro studies with human corneal epithelial cells (HCEpi) also showed that IKKβ was required for cytokine-induced cell migration and wound closure but was dispensable for cell proliferation. In both in vivo and in vitro settings, IKKβ was required for optimal activation of NF-κB and p38 signaling in corneal epithelial cells, and p38 activation is likely mediated through formation of an IKKβ-p38 protein complex. Thus, our studies in corneal epithelium reveal a previously un-recognized role for IKKβ in the control of epithelial cell motility and wound healing

Expression of signaling components in embryonic eyelid epithelium.

Closure of an epithelium opening is a critical morphogenetic event for development. An excellent example for this process is the transient closure of embryonic eyelid. Eyelid closure requires shape change and migration of epithelial cells at the tip of the developing eyelids, and is dictated by numerous signaling pathways. Here we evaluated gene expression in epithelial cells isolated from the tip (leading edge, LE) and inner surface epithelium (IE) of the eyelid from E15.5 mouse fetuses by laser capture microdissection (LCM). We showed that the LE and IE cells are different at E15.5, such that IE had higher expression of muscle specific genes, while LE acquired epithelium identities. Despite their distinct destinies, these cells were overall similar in expression of signaling components for the "eyelid closure pathways". However, while the LE cells had more abundant expression of Fgfr2, Erbb2, Shh, Ptch1 and 2, Smo and Gli2, and Jag1 and Notch1, the IE cells had more abundant expression of Bmp5 and Bmpr1a. In addition, the LE cells had more abundant expression of adenomatosis polyposis coli down-regulated 1 (Apcdd1), but the IE cells had high expression of Dkk2. Our results suggest that the functionally distinct LE and IE cells have also differential expression of signaling molecules that may contribute to the cell-specific responses to morphogenetic signals. The expression pattern suggests that the EGF, Shh and NOTCH pathways are preferentially active in LE cells, the BMP pathways are effective in IE cells, and the Wnt pathway may be repressed in LE and IE cells via different mechanisms

A BIM technology-based underwater structure damage identification and management method

With the continuous development of bridge technology, the condition assessment of large bridges has gradually attracted attention. Structural Health Monitoring (SHM) technology provides valuable information about a structure's existing health, keeping it safe and uninterrupted use under various operating conditions by mitigating risks and hazards on time. At the same time, the problem of bridge underwater structure disease is becoming more obvious, affecting the safe operation of the bridge structure. It is necessary to test the bridge’s underwater structure. This paper develops a bridge underwater structure health monitoring system by combining building information modeling (BIM) and an underwater structure damage algorithm. This paper is verified by multiple image recognition networks, and compared with the advantages of different networks, the YOLOV4 network is used as the main body to improve, and a lightweight convolutional neural network (Lite-yolov4) is built. At the same time, the accuracy of disease identification and the performance of each network are tested in various experimental environments, and the reliability of the underwater structure detection link is verified

MAP3K1 function is essential for cytoarchitecture of the mouse organ of Corti and survival of auditory hair cells

MAP3K1 is a serine/threonine kinase that is activated by a diverse set of stimuli and exerts its effect through various downstream effecter molecules, including JNK, ERK1/2 and p38. In humans, mutant alleles of MAP3K1 are associated with 46,XY sex reversal. Until recently, the only phenotype observed in Map3k1tm1Yxia mutant mice was open eyelids at birth. Here, we report that homozygous Map3k1tm1Yxia mice have early-onset profound hearing loss accompanied by the progressive degeneration of cochlear outer hair cells. In the mouse inner ear, MAP3K1 has punctate localization at the apical surface of the supporting cells in close proximity to basal bodies. Although the cytoarchitecture, neuronal wiring and synaptic junctions in the organ of Corti are grossly preserved, Map3k1tm1Yxia mutant mice have supernumerary functional outer hair cells (OHCs) and Deiters' cells. Loss of MAP3K1 function resulted in the downregulation of Fgfr3, Fgf8, Fgf10 and Atf3 expression in the inner ear. Fgfr3, Fgf8 and Fgf10 have a role in induction of the otic placode or in otic epithelium development in mice, and their functional deficits cause defects in cochlear morphogenesis and hearing loss. Our studies suggest that MAP3K1 has an essential role in the regulation of these key cochlear morphogenesis genes. Collectively, our data highlight the crucial role of MAP3K1 in the development and function of the mouse inner ear and hearing

Expression of Genes in the FGF pathways

<p>Expression of Genes in the FGF pathways</p

Expression of genes in the Wnt pathways

<p>Expression of genes in the Wnt pathways</p

Myofibroblast transformation, senescence and apoptosis of the injured cornea.

<p>(A) The <i>Ikkβ</i>^<i>F</i> and <i>Ikkβ</i> ^<i>ΔCS</i> eyes were harvested at 28 days after alkali burn injury. The tissues were processed and used for immunohistochemistry using anti-α-SMA, a marker for myofibroblast and TUNEL assays for the detection of apoptotic cells. Blue: DAPI (nuclei), Red: leukocytes. (B) The <i>Ikkβ</i>^<i>F</i> and <i>Ikkβ</i> ^<i>ΔCS</i> eyes were harvested at 4 days and 28 days after alkali burn injury. The tissue sections were examined by SA-β-Gal staining. The SA-β-Gal positive cells are stained with blue color. ST: corneal stroma, EP, corneal epithelium, labeled with arrows. (B and D) The number of staining positive cells was quantified and **p<0.01 and ***p<0.001 was considered significantly different between <i>Ikkβ</i>^<i>F</i> and <i>Ikkβ</i> ^<i>ΔCS</i> eyes. Data represent at least at least 5 slides/eye and 3 injured eyes examined.</p

Corneal Wound Healing Requires IKB kinase β Signaling in Keratocytes

<div><p>IkB kinase β (IKKβ) is a key signaling kinase for inflammatory responses, but it also plays diverse cell type-specific roles that are not yet fully understood. Here we investigated the role of IKKβ in the cornea using <i>Ikkβ</i>^<i>ΔCS</i> mice in which the <i>Ikkβ</i> gene was specifically deleted in the corneal stromal keratocytes. The <i>Ikkβ</i>^<i>ΔCS</i> corneas had normal morphology, transparency and thickness; however, they did not heal well from mild alkali burn injury. In contrast to the <i>Ikkβ</i>^<i>F/F</i> corneas that restored transparency in 2 weeks after injury, over 50% of the <i>Ikkβ</i>^<i>ΔCS</i> corneas failed to fully recover. They instead developed recurrent haze with increased stromal thickness, severe inflammation and apoptosis. This pathogenesis correlated with sustained myofibroblast transformation with increased α smooth muscle actin (α-SMA) expression, higher levels of senescence β-Gal activity and scar tissue formation at the late stage of wound healing. In addition, the <i>Ikkβ</i>^<i>ΔCS</i> corneas displayed elevated expression of hemo-oxygenase-1 (HO-1), a marker of oxidative stress, and activation of stress signaling pathways with increased JNK, c-Jun and SMAD2/3 phosphorylation. These data suggest that IKKβ in keratocytes is required to repress oxidative stress and attenuate fibrogenesis and senescence in corneal wound healing.</p></div